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Background:
Traditional measures of obesity, like body mass index (BMI) and waist circumference, have been linked to ADHD risk — but they aren’t great at capturing where fat is actually stored in the body. A newer index called relative fat mass (RFM), which combines height and waist circumference, does a better job of estimating overall body fat and predicting metabolic risks like heart disease and metabolic syndrome. Because those conditions share some underlying biological mechanisms with ADHD, researchers wondered whether RFM might also help explain the relationship between obesity and ADHD — particularly in children.
That question is complicated by the fact that ADHD doesn't look the same in boys and girls. Boys tend to display more hyperactive and impulsive behavior, making their ADHD easier to spot. Girls more often show inattention, which is quieter and frequently goes undiagnosed.
The Study:
A new study set out to test whether RFM is associated with ADHD in children, and whether that association differs between sexes. Using data from the National Health and Nutrition Examination Survey (NHANES) collected between 1999 and 2004, the researchers narrowed a large initial pool of over 31,000 participants down to 5,089 children and adolescents aged 6 to 14 who had complete data on height, waist circumference, ADHD screening, and other relevant variables.
After adjusting for age, race/ethnicity, Poverty-Income Ratio, maternal age at delivery, maternal smoking during pregnancy, health insurance coverage, and birth weight, the results revealed a striking split along sex lines.
In boys, higher RFM was associated with lower odds of ADHD. Compared to boys in the lowest fat-mass quartile, those in the second quartile had about 10% lower odds of ADHD, rising to over 30% lower in the third quartile and nearly 40% lower in the highest. In girls, the pattern reversed entirely. While girls in the second quartile showed similar odds to those with the lowest RFM, girls in the third and fourth quartiles had 60% to 70% greater odds of ADHD.
Conclusion & Why This Matters:
In recent years, the relationship between obesity and ADHD has become an increasingly important focus in pediatric neurodevelopmental research. Studies have reported higher rates of ADHD symptoms among children and adolescents with obesity compared with their non-obese peers, and difficulties with peer relationships have also been linked to increased obesity risk (Sönmez et al., 2019). From a neurobiological standpoint, both conditions may involve shared underlying mechanisms, particularly dysfunction in dopaminergic pathways.
The authors concluded that higher body fat levels appear to lower ADHD risk in boys while raising it in girls. This finding highlights why sex-specific analysis matters in ADHD research. The underlying biological reasons for this divergence, however, remain an open question and open the door for future research.
Sitong Bi, Huijing Li, Xinyang Xu, and Lihua Li, “Sex-Specific Effects of Relative Fat Mass on Attention-Deficit/Hyperactivity Disorder: Insights from the 1999–2004 National Health and Nutrition Examination Survey,” Journal of Child and Adolescent Psycopharmacology (2026), https://doi.org/10.1177/10445463261416680.
Executive function impairment is a key feature of ADHD, with its severity linked to the intensity of ADHD symptoms. Executive function involves managing complex cognitive tasks for organized behavior and includes three main areas: inhibitory control (suppressing impulsive actions), working memory (holding information briefly), and cognitive flexibility (switching between different mental tasks). Improving executive functions is a critical objective in the management of ADHD.
Recent studies show that exercise interventions can enhance executive function in individuals with ADHD. Unlike traditional medications, which are costly and may cause side effects such as headaches, nausea, or growth issues, exercise can be incorporated into daily routines of children and adolescents without negative reactions.
Some studies report that aerobic exercise does not significantly improve executive function. However, most past reviews of aerobic exercise effects on executive function have focused on people without ADHD, with few examining interventions for children or adolescents with ADHD.
The Study:
A Chinese and South Korean study team conducted a systematic search of the peer-reviewed published literature to perform meta-analyses on randomized controlled trials (RCTs) specifically focused on aerobic exercise interventions for children and adolescents with ADHD.
All studies included were randomized controlled trials involving participants aged 6 to 18 years who had been clinically diagnosed with ADHD. The interventions consisted of various forms of aerobic exercise, while the control groups engaged in either non-exercise activities or daily routines. Each study was required to report at least one outcome measure with usable data for calculating the effect size on executive functioning.
The Results:
Meta-analysis of fifteen RCTs combining 653 children and adolescents with ADHD reported a medium to large effect size improvement in inhibitory control. There was no sign of publication bias, but wide heterogeneity (variation) in outcomes among studies.
Six to eight weeks of aerobic exercise produced modest improvements, with much greater gains seen after twelve weeks. Hour-long sessions were as effective as longer ones. Moderate intensity exercise proved more beneficial than vigorous intensity.
Meta-analysis of eight RCTs combining 399 children and adolescents with ADHD produced a medium effect size improvement in working memory. There was no sign of publication bias, and heterogeneity was moderate.
Once again, six to eight weeks of aerobic exercise produced modest improvements, with much greater gains seen after twelve weeks. Hour-long sessions were as effective as longer ones. But in this case moderate-to-vigorous intensity yielded the best results.
Meta-analysis of ten RCTs combining 443 children and adolescents with ADHD was associated with a medium to large effect size improvement in cognitive flexibility. There was no sign of either publication bias or heterogeneity. Neither the length of treatment, session time, or intensity affected the outcome.
The Take-Away:
The team concluded, “Our study indicates that aerobic exercise interventions have a positive impact with a moderate effect size on inhibitory control, working memory, and cognitive flexibility in children and adolescents with ADHD. However, the effectiveness of the intervention is influenced by factors such as the intervention period, frequency, session durations, intensity, and the choice between acute or chronic exercise. Specifically, chronic aerobic exercise interventions lasting 12 weeks or longer, with a frequency of 3 to 5 sessions per week, session durations of 60 min or more, and intensities that are moderate or moderate-to-vigorous, have the greatest overall effect… caution should be exercised when interpreting these findings due to the significant heterogeneity in inhibitory control and working memory.”
After noting that the association between ADHD and obesity has been called into question because of small sample sizes, wide age ranges, self-reported assessments, and inadequate attention to potential confounders, an Israeli study team set out "to assess the association between board-certified psychiatrist diagnoses of ADHD and measured adolescent BMI [body mass index] in a nationally represented sample of over one million adolescents who were medically evaluated before mandatory military service."
The team distinguished between severe and mild ADHD. It also focused on a single age group.
All Israelis are subject to compulsory military service. In preparation for that service, military physicians perform a thorough medical evaluation. Trained paramedics recorded every conscript's height and weight.
The study cohort was divided into five BMI percentile groups according to the U.S. Centers for Disease Control and Prevention's BMI percentiles for 17-year-olds, and further divided by sex: <5th percentile (underweight), 5th-49th percentile (low-normal), 50th-84th percentile (high normal), 85th-94th percentile (overweight) and ≥95th (obese). Low-normal was used as the reference group.
Adjustments were made for sex, birth year, age at examination, height, country of birth (Israeli or other), socioeconomic status, and education level.
In the fully adjusted results, those with severe ADHD were 32% more likely to be overweight and 84% more likely to be obese than their typically developing peers. Limiting results to Israeli-born conscripts made a no difference.
Male adolescents with mild ADHD were 24% more likely to be overweight, and 42% more likely to be obese. Females with mild ADHD are 33% more likely to be overweight, and 42% more likely to be obese. Again, the country of birth made no difference.
The authors concluded, that both severe and mild ADHD was associated with an increased risk for obesity in adolescents at the age of 17 years. The increasing recognition of the persistence of ADHD into adulthood suggests that this dual morbidity may have a significant impact on the long-term health of individuals with ADHD, thus early preventive measures should be taken.
The Background:
Concerns remain about how ADHD and methylphenidate (MPH) use might affect children's health and growth, and especially how it may affect their adult height. While some studies suggest disrupted growth and a possible biological mechanism, the impact of ADHD prevalence and MPH use is still unclear. Children with ADHD may develop unhealthy habits – irregular eating, low physical activity, and poor sleep – that can contribute to obesity and reduced height. MPH’s appetite-suppressing effect can lead to skipped meals or overeating. Since growth hormone is mainly released during deep sleep, chronic sleep deprivation could plausibly slow growth and impair height development; however, a clear link between ADHD, MPH use, overweight, and shorter stature has never been firmly established.
The Study:
South Korea has a single payer health insurance system that covers more than 97% of its population. A Korean research team used the National Health Insurance Service database to perform a nationwide population study to explore this topic further.
The study involved 34,850 children, of whom 12,866 were diagnosed with ADHD. Of these children, 6,816 (53%) had received methylphenidate treatment, while 6,050 (47%) had not. Each patient with ADHD was precisely matched 1:1 by age, sex, and income level to a control participant without ADHD. The sex ratio was comparable in all groups.The team used Body Mass Index (BMI) as an indicator of overweight and obesity.
The Results:
The researchers found that being diagnosed with ADHD was associated with 50% greater odds of being overweight or obese as young adults, and over 70% greater odds of severe obesity (BMI > 30) compared to matched non-ADHD controls, regardless of whether or not they were medicated.
Those diagnosed with ADHD, but not on methylphenidate, had 40% greater odds of being overweight or obese, and over 55% greater odds of becoming severely obese, relative to matched non-ADHD controls.
Methylphenidate users had 60% greater odds of being overweight or obese, and over 85% greater odds of becoming severely obese, relative to matched non-ADHD controls.
There were signs of a dose-response effect. Less than a year’s exposure to methylphenidate was associated with roughly 75% greater odds of becoming severely obese, whereas exposure over a year or more raised the odds 2.3-fold, relative to matched non-ADHD controls. Using MPH increased the prevalence of overweight from 43.2% to 46.5%, with a greater prevalence among those using MPH for more than one year (50.5%).
It is important to note that most of this effect was from ADHD itself, with methylphenidate only assuming a predominant role in severe obesity among those with longer-term exposure to the medicine.
As for height, children with ADHD were no more likely to be short of stature than matched non-ADHD controls. Being prescribed methylphenidate was associated with slightly greater odds (7%) of being short of stature, but there was no dose-response relationship.
Conclusion:
The team concluded, “patients with ADHD, particularly those treated with MPH, had a higher BMI and shorter height at adulthood than individuals without ADHD. Although the observed height difference was clinically small in both sexes and age groups, the findings suggest that long-term MPH exposure may be associated with growth and body composition, highlighting the need for regular monitoring of growth.” They also point out that “Despite these findings, the clinical relevance should be interpreted with caution. In our cohort, the mean difference in height was less than 1 cm (eg, maximum −0.6 cm in females) below commonly accepted thresholds for clinical significance.” Likewise, increases in overweight/BMI were small.
One problem with interpreting the BMI/obesity results is that some of the genetic variants that cause ADHD also cause obesity. If that genetic load increases with severity of ADHD than the results from this study are confounded because those with more severe ADHD are more likely to be treated than those with less severe ADHD.
Due to these small effects along with the many study limitations noted by the authors, these results should be considered alongside the well-established benefits of methylphenidate treatment.
Antidepressants are the primary drug treatment for depressive disorders, which affect 15–20% of pregnant women. They are among the most widely prescribed medications worldwide, and their use has increased in recent decades. Understanding their reproductive safety is critical to support informed, evidence-based prescribing during pregnancy.
A new meta-analysis sheds important light on one of the most debated concerns: whether children born to mothers who took antidepressants during pregnancy face a higher risk of ADHD.
The Study:
Pooling 14 studies covering more than 14 million participants, the analysis found that prenatal antidepressant exposure was associated with a 35% higher rate of ADHD in offspring compared to no exposure. A separate look at SSRIs (the most widely prescribed class of antidepressants, including Prozac and Zoloft) across 11 studies and over four million pregnancies found an even higher apparent risk (44%) after correcting for publication bias. On the surface, these are striking numbers.
Both associations came with an important caveat: enormous variation between individual studies, a statistical red flag suggesting the results may not reflect a true underlying effect. More tellingly, the apparent risk evaporated entirely when researchers applied a more rigorous method — comparing siblings within the same family, where one child was exposed to antidepressants in the womb, and another was not.
This sibling-comparison design is particularly powerful because it automatically controls for factors that run in families: shared genes, household environment, parenting, and socioeconomic conditions. When those influences are held constant, the link between antidepressant exposure and ADHD disappears. The same pattern held for SSRIs specifically.
Two other antidepressant classes, SNRIs (serotonin norepinephrine reuptake inhibitors) and tricyclics, showed no significant association in any analysis.
“Confounding by Indication”:
The probable driver of the initial association is what researchers call confounding by indication. The very condition being treated (depression) is itself a risk factor for ADHD in offspring, independently of any medication. Mothers with more severe depression are also more likely to be prescribed antidepressants, meaning the drug and the underlying illness are difficult to disentangle in standard analyses. Sibling studies cut through this problem cleanly.
The Take-Away:
The authors concluded that the association between antidepressants and ADHD risk was non-significant across all analyses designed to account for these confounding factors. This doesn’t mean antidepressants are without any reproductive considerations, but it does suggest that ADHD risk, at least, is driven by heritable and family-level factors rather than medication exposure itself.
For clinicians and patients weighing the risks of treating or not treating depression during pregnancy, this distinction matters considerably.
Executive functions are the mental processes that allow us to plan, adapt, and follow through. This encompasses working memory, inhibitory control, cognitive flexibility, goal-directed planning, and problem-solving. In people with ADHD, weaknesses in these areas compound the disorder's core symptoms, making it substantially harder to manage complex, real-world demands.
Background:
Medication remains the frontline clinical response. Stimulant medications can meaningfully reduce both executive function deficits and ADHD symptoms, and are often combined with behavioral or psychological therapies for better overall outcomes.
Medication, however, is not entirely without risk of side effects. These risks have spurred interest in new, non-pharmacological alternatives that target the same neural pathways. One of these new therapies is Computerized Cognitive Remediation Therapy (CCRT). This therapy uses digital programs delivered via computer, tablet, or smartphone that train attention, memory, and inhibitory control through structured cognitive exercises. A key feature of many CCRT platforms is adaptive difficulty: tasks adjust in real time to match the child’s current ability, keeping training both challenging and engaging.
The Study:
Despite this promise, the evidence base in younger populations has been limited. This meta-analysis pooled results from randomized controlled trials enrolling participants under 18 who either carried an ADHD diagnosis or scored above the threshold on a validated rating scale. Comparators included no treatment (waitlist), placebo (pharmacological or psychological), or treatment as usual. The primary outcomes (overall executive function and clinical symptom severity) were assessed via questionnaires and neuropsychological testing. Studies including participants with comorbid autism, tic disorders, epilepsy, or other psychiatric conditions were excluded.
The findings were informative, but overall results were mixed. CCRT produced a small but statistically meaningful reduction in inattention symptoms across 13 studies (885 participants), with consistent results across individual trials and no evidence of publication bias. However, it had no detectable effect on hyperactivity and impulsivity (12 studies, 833 participants) or on total ADHD symptom burden (10 studies, 731 participants).
The picture was more encouraging for executive function. Nine studies (500 participants) showed small overall improvements, with specific gains in working memory (454 participants), inhibitory control (428 participants), and planning (6 studies, 335 participants). Emotional control showed no significant change (5 studies, 265 participants), nor did cognitive flexibility (4 studies, 189 participants).
The Take-Away:
Taken together, these results are modest rather than transformative, but context matters. CCRT is low-cost, digitally scalable, and carries negligible side effects. For a population where medication often comes with a significant burden of adverse reactions, even small, reliable improvements in executive function represent a meaningful clinical option.
The evidence positions CCRT not as a replacement for established treatments, but as a practical and well-tolerated addition to the therapeutic toolkit for children and adolescents with 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.
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