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June 10, 2025
This new meta-analysis confirms what other meta-analysis have already shown, i.e, that there exists in the population an association between maternal smoking during pregnancy and ADHD in their offspring. But reader beware, association does not mean causation.
The team identified 55 studies with quantitative data suitable for meta-analysis, including 11 case-control, 13 cross-sectional, and 31 retrospective/prospective cohort studies.
Altogether they combined more than four million persons in countries spanning six continents, including the United States, Finland, Sweden, Brazil, the Netherlands, Japan, the UK, Spain, China, Australia, New Zealand, Norway, Canada, France, Sweden, South Korea, Turkey, Romania, Bulgaria, Lithuania, Germany, Denmark, Egypt, and India.
Meta-analysis of all 55 studies found that offspring of mothers who smoked tobacco during pregnancy were about 70% more likely to develop ADHD than offspring of mothers who did not smoke during pregnancy.
Because variation in outcomes across studies was very high, the team performed subgroup analyses to explore potential sources of this heterogeneity.
Comparing study designs, cohort studies reported roughly 50% greater odds of ADHD among children of mothers who smoked during pregnancy, whereas case-control studies reported roughly 70% greater odds and cross-sectional studies 2.3-fold greater odds.
Studies using the most reliable method of determining ADHD – clinical interview/professional diagnosis – reported 90% greater odds, contrasting with 66% through medical records/databases and 58% through self-report by child/parent or through teacher report.
Good quality studies reported roughly 75% greater odds.
Studies with sample sizes above two thousand similarly found 70% greater odds.
There was no sign of publication bias using the more commonly used Egger’s test, but a marginal indication of publication bias using Begg’s test. Performing a standard correction reduced the effect size, indicating that the offspring of mothers who smoked tobacco during pregnancy were over 50% more likely to develop ADHD than the offspring of mothers who did not smoke during pregnancy.
The team concluded, “This systematic review and meta-analysis of 55 studies, encompassing over four million participants, provides compelling evidence that maternal tobacco smoking during pregnancy significantly increases the odds of ADHD in children … These findings underscore the critical need for public health interventions aimed at reducing tobacco smoking during pregnancy.”
However, we disagree with this conclusion; The authors ignore substantial evidence showing that maternal smoking during pregnancy is confounded by maternal ADHD. These mothers transmit ADHD via genetics, not via their smoking. This study should be seen not as "...[further evidence that smoking during pregnancy causes ADHD.] ", but as a lesson in how easy it can be to see correlation as causation.
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Mahdi Mohammadian, Lusine G. Khachatryan, Filipp V. Vadiyan, Mostafa Maleki, Fatemeh Fatahian, and Abdollah Mohammadian-Hafshejani, “The association between maternal tobacco smoking during pregnancy and the risk of attention-deficit/hyperactivity disorder (ADHD) in offspring: A systematic review and meta-analysis,” PLOS ONE (2025), 20(2): e0317112, https://doi.org/10.1371/journal.pone.0317112.
A Swedish-Danish-Dutch team used the Swedish Medical Birth Register to identify the almost 1.7 million individuals born in the country between 1980 and 1995. Then, using the Multi-Generation Register, they identified 341,066 pairs of full siblings and 46,142 pairs of maternal half-siblings, totaling 774,416 individuals.
The team used the National Patient Register to identify diagnoses of ADHD, as well as neurodevelopmental disorders (autism spectrum disorder, developmental disorders, intellectual disability, motor disorders), externalizing psychiatric disorders (oppositional defiant and related disorders, alcohol misuse, drug misuse), and internalizing psychiatric disorders (depression, anxiety disorder, phobias, stress disorders, obsessive-compulsive disorder).
The team found that ADHD was strongly correlated with general psychopathology overall (r =0.67), as well as with the neurodevelopmental (r = 0.75), externalizing (r =0.67), and internalizing (r = 0.67) sub factors.
To tease out the effects of heredity, shared environment, and non-shared environment, a multivariate correlation model was used. Genetic variables were estimated by fixing them to correlate between siblings at their expected average gene sharing (0.5for full siblings, 0.25 for half-siblings). Non-genetic environmental components shared by siblings (such as growing up in the same family) were estimated by fixing them to correlate at 1 across full and half-siblings. Finally, non-shared environmental variables were estimated by fixing them to correlate at zero across all siblings.
This model estimated the heritability of the general psychopathology factor at 49%, with the contribution of the shared environment at 7 percent and the non-shared environment at 44%. After adjusting for the general psychopathology factor, ADHD showed a significant and moderately strong phenotypic correlation with the neurodevelopmental-specific factor (r = 0.43), and a significantly smaller correlation with the externalizing-specific factor (r = 0.25).
For phenotypic correlation between ADHD and the general psychopathology factor, genetics explained 52% of the total correlation, the non-shared environment 39%, and the shared familial environment only 9%. For the phenotypic correlation between ADHD and the neurodevelopmental-specific factor, genetics explained the entire correlation because the other two factors had competing effects that canceled each other out. For the phenotypic correlation between ADHD and the externalizing-specific factor, genetics explained 23% of the correlation, shared environment 22%, and non-shared environment 55%.
The authors concluded that "ADHD is more phenotypically and genetically linked to neurodevelopmental disorders than to externalizing and internalizing disorders, after accounting for a general psychopathology factor. ... After accounting for the general psychopathology factor, the correlation between ADHD and the neurodevelopmental-specific factor remained moderately strong, and was largely genetic in origin, suggesting substantial unique sharing of biological mechanisms among disorders. In contrast, the correlation between ADHD and the externalizing-specific factor was much smaller and was largely explained by-shared environmental effects. Lastly, the correlation between ADHD and the internalizing subfactor was almost entirely explained by the general psychopathology factor. This finding suggests that the comorbidity of ADHD and internalizing disorders are largely due to shared genetic effects and non-shared environmental influences that have effects on general psychopathology."
A recent CNN report, http://tinyurl.com/yannlfd6, highlighted a paper published in Pediatrics, which reported that pregnant women who use acetaminophen during pregnancy put their unborn child at two-fold increased risk for attention deficit hyperactivity disorder (ADHD). In that study, acetaminophen use during pregnancy was common; nearly half of women surveyed used the painkiller during pregnancy. Other studies have reported similar associations of acetaminophen, also known as paracetamol with ADHD or with other problems in childhood (e.g., https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5300094/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4177119/, https://www.ncbi.nlm.nih.gov/pubmed/24566677, https://www.ncbi.nlm.nih.gov/pubmed/24163279). Given these prior findings, it seems unlikely that the new report is a chance finding. But does it make any biological sense? One answer to that question came from an epigenetic study. Such studies figure out if assaults from the environment change the genetic code. One epigenetic study found that prenatal exposure changes the fetal genome via a process called methylation. Such genomic changes could increase the risk for ADHD (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5540511/). Because all of these studies are observational studies, one cannot assert with certainty that there is a causal link between acetaminophen use during pregnancy.
The observed association could be due to some unmeasured third factor. Although the researchers did a respectable job ruling out some third factors, we must acknowledge some uncertainty in the finding. That said, what should pregnant women do if they need acetaminophen. I suggest you bring this information to your physician and ask if there is a suitable alternative.
Secondhand smoke (SHS) is tobacco smoke inhaled by nonsmokers sharing enclosed spaces with smokers. It contains well over two hundred toxic chemicals, including some toxic metals known to cause serious harm to humans. It is among the most common indoor air pollutants worldwide, with roughly two in five children exposed.
Until now, studies have focused primarily on maternal smoking before childbirth. A Chinese research team set out to explore what, if any, association there might be between childhood exposure to SHS and ADHD. They conducted a comprehensive search of the peer-reviewed literature and identified nine studies with a combined total of over a hundred thousand participants that looked for such effects. The studies were carried out in the United States, Germany, Spain, and the Republic of Korea.
Merging these studies into a meta-analysis, the team found that children exposed to secondhand smoke were 60 percent more likely to develop ADHD. The same overall pattern held true on all three continents.
A further meta-analysis of four of the studies with over 12,000 participants found children exposed to secondhand smoke were 33% more likely to exhibit conduct problems.
The authors concluded, "The results of our meta-analysis suggest that postnatal exposure to SHS may be associated with ADHD in children. Exposure to SHS can also lead to a variety of adverse behavioral outcomes in children. Therefore, parents should stop smoking to create a good growing environment for their children. Further prospective studies should fully adjust for potential confounding factors to determine whether there is a causal relationship between SHS and ADHD."
If you or someone you know has ADHD, you may be familiar with the challenge of staying on medication. Stimulants like methylphenidate (Ritalin) are the most common and effective treatment for ADHD, but a surprisingly large number of people stop taking them within the first year. In our new study, published in Translational Psychiatry, we sought to determine whether a person's genetic makeup plays a role in the development of the disorder.
What We Did
We analyzed data from over 18,000 people with ADHD in Denmark, all of whom had started stimulant medication. We tracked whether they stopped treatment within the first year, defined as going more than six months without filling a prescription. Nearly 4 in 10 (39%) had discontinued by that point. We then looked at their genetic data to see whether DNA differences could help explain who was more likely to stop.
What We Found
The short answer is: genetics does play a role, but it's modest. No single gene had a dramatic effect. Instead, we found that a collection of small genetic influences—distributed across the genome—contributed to the likelihood of stopping treatment early.
One of the most consistent findings was that people with a higher genetic predisposition for psychiatric disorders like schizophrenia, depression, or general mental health difficulties were more likely to discontinue their medication. This was true across all age groups. Interestingly, having a higher genetic risk for ADHD itself was not associated with stopping treatment, suggesting that the genetics of having ADHD and the genetics of staying on medication are quite different things.
We also found that the genetic picture looks different depending on age. In children under 16, body weight genetics (BMI) played a surprising role, children with a genetic tendency toward higher weight were actually less likely to stop, possibly because stimulant-related appetite suppression is less of a problem for them. In older adolescents and adults, higher genetic potential for educational attainment and IQ was linked to staying on treatment, possibly reflecting better access to information and healthcare support.
On the rare variant side, we found a tentative signal that people who stopped treatment had fewer disruptive variants in genes involved in dopamine, the brain chemical that stimulants work on. This might mean that those who continue on medication genuinely have more disruption in their dopamine system and benefit more from stimulant treatment.
What This Means
Our findings suggest that stopping ADHD medication early isn't simply a matter of willpower or forgetting to take a pill. Biology matters. A person's broader genetic vulnerabilities, particularly for other psychiatric disorders, may make it harder to stay on treatment, perhaps because of side effects, poor response, or the complexity of managing multiple mental health challenges at once.
We're still far from being able to use genetics to predict who will stop their medication, the effects we found are real but small, and much of the variation in treatment persistence remains unexplained. But this work is a step toward understanding the biological foundations of treatment challenges in ADHD, and hopefully toward more personalized approaches to care in the future.
Larger studies and research that can distinguish why people stop (side effects versus poor response versus practical barriers), will be the next steps.
ADHD affects both individuals and society in many ways. Children and adolescents with ADHD often struggle with focusing, controlling impulses, and staying organized, which leads to problems with schoolwork, learning, and taking tests. These challenges can cause academic failure and make it harder for them to stay in school.
ADHD symptoms often continue into adulthood, affecting jobs, relationships, and increasing risks for substance abuse and legal problems.
Families of children and adolescents with ADHD face extra stress, with parents more likely to experience depression, anxiety, and relationship difficulties. The economic impact is also large, with billions spent each year on medical care, special education, lost productivity, and other related costs.
Current treatments for ADHD mostly include medication, behavioral therapy, and educational support. While medications like stimulants can help control ADHD symptoms in the short term, they often cause side effects such as loss of appetite, trouble sleeping, slowed growth, cardiovascular risks, and potential substance dependence. These issues can make it hard for children and adolescents to stay on their medication, and about a third either don’t respond well or can’t tolerate the side effects. Once medication is stopped, the benefits fade quickly and do not lead to lasting improvements in executive functions (thinking skills).
Behavioral therapy and parent training can help with behavior problems, but have limited effects on core mental skills like planning and self-control. These approaches also tend to be expensive, require a lot of support from parents and teachers, and are hard to use widely in schools and communities that lack resources.
Recently, exercise interventions have attracted growing interest as a non-pharmacological option. They provide several benefits: no drug-related side effects, easy accessibility, low cost, simple implementation in schools and communities, and enhanced physical and mental health.
Previous meta-analyses examining how exercise interventions affect children and adolescents with ADHD have used traditional univariate models, which treat each study as if it only offers one independent effect size. In contrast, this study used multilevel meta-analysis — a more advanced statistical method modelling both between-study and within-study effects. This approach results in more accurate estimates and more dependable conclusions.
Eligible studies were randomized controlled trials (RCTs) with usual care, no intervention, or waitlist controls, involving children and adolescents aged 5–18 diagnosed with ADHD by internationally recognized diagnostic criteria, and reporting inhibitory control outcomes.
Eleven studies combining 512 children and adolescents met these inclusion standards.
The analysis between experimental and control groups indicated that the exercise intervention group had significantly improved inhibitory control performance compared to the control group, with a medium-to-large effect size. There was very little variation (heterogeneity) in outcome between the studies, and no sign of publication bias.
Within-group analyses showed that experimental groups had significant improvements after the intervention compared to baseline, with large effect sizes and moderate heterogeneity.
By comparison, analyzing control groups over the same period revealed no significant differences, indicating that inhibitory control abilities in these groups remained largely unchanged throughout the observation period. There was little heterogeneity.
Nevertheless, only one of the studies was rated low risk of bias, nine had some concerns, and two were rated high risk of bias. The greatest shortcomings were a lack of blinding and preregistration.
The study authors therefore concluded that the overall evidence quality of this meta-analysis is low, limiting confidence in the results. While exercise interventions seem to improve inhibitory control abilities in children and adolescents with ADHD, significant methodological limitations create uncertainty about the effect size. These require more rigorous future studies to clarify these effects. Despite these caveats, they noted that all included studies reported statistically significant, consistent benefits from exercise interventions, offering preliminary support for their use as an adjunctive approach.
Takeaway
This study lands in the same conversation as the adult ADHD exercise meta-analysis, and together they start to form a coherent picture: exercise appears to support attention and impulse control across the lifespan for people with ADHD, not just in one age group. The honest caveat is that the research quality in this field is still catching up to the enthusiasm — most studies have design weaknesses that limit confidence in the exact size of the effect. But the consistency of findings across studies, age groups, and now two separate meta-analyses is hard to dismiss.
A new study in the respected journal PLOS One analyzes data from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) to examine trends in the incidence, prevalence, and disability-adjusted life-years associated with ADHD among adolescents and young adults aged 10 to 24 years between 1990 and 2021.
The GBD 2021, released by the Institute for Health Metrics and Evaluation (U.S.), is a comprehensive global analysis of 371 diseases, injuries, and risk factors – such as ADHD – across 204 countries from 1990 to 2021. Its open-source data are publicly available.
First, a distinction. Incidence measures the number of new cases of a disease that develop in a specific population each year. Prevalence measures the total number of existing cases – both new and pre-existing – in a population each year.
The estimated global incidence of ADHD declined marginally from 12.61 per 100,000 population in 1990 to 11.89 per 100,000 population in 2021, representing an average annual decrease of 0.6% in age-standardized incidence. The rates observed were comparable between males and females.
Regional trends varied: Western Europe had the highest rise in ADHD incidence (0.5% annually), while North Africa and the Middle East saw the largest drop (0.7% annually). Overall, a higher Socio-Demographic Index (SDI) is linked to a greater incidence, although it is far from a perfect fit. Nationally, showed the highest increase in ADHD incidence (1.15% annually), while Qatar showed the largest decrease with an annualized reduction of 1.77%.
The estimated global prevalence of ADHD declined marginally from 2.38% in 1990 to 2.17% in 2021. Again, the decline was similar for males and females, and across all age groups (10-14, 15-19, 20-24). Higher SDI was associated with higher prevalence, but inconsistently.
Disability-adjusted life-years (DALYs) combine years lost from early death and years lived with disability to measure disease burden. Globally, the age-standardized DALYs rate for ADHD decreased slightly from 30.3 per 100,000 population to 26.6 per 100,000 population, for an average annual decline of 0.6%. The decline occurred across age groups and was similar between males and females.
The authors concluded that ADHD rates and related health burdens have generally declined over the past quarter century, though recent patterns are less consistent due to factors like socioeconomic changes and evolving diagnostic standards. Continued research is needed to improve the accuracy and accessibility of ADHD diagnosis and treatment to further reduce its global impact.
Take-Away:
The broader takeaway is one of cautious reassurance. Despite rising public awareness and diagnosis rates in many Western countries, the global picture over 25 years shows a gentle decline in ADHD burden among young people as opposed to a crisis of escalating proportions as social media may make one think. That said, the variation between regions suggests that access to diagnosis, cultural factors, and reporting standards are shaping the numbers as much as underlying biology. Progress is real but uneven, and the work of improving equitable access to diagnosis and care is far from finished.
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