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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."
A recent meta-analysis examined how well cognitive behavioral therapy (CBT) improves not just symptoms, but everyday functioning and quality of life in adults with ADHD.
The Background:
ADHD in adults affects far more than attention or impulsivity. It often disrupts key areas of life:
These broad impacts highlight a key issue: reducing symptoms does not automatically translate into better day-to-day functioning.
CBT is a structured, skills-based therapy that helps people:
While both medication (especially stimulants) and CBT improve core ADHD symptoms, CBT is particularly aimed at improving real-world functioning.
The Study:
The researchers analyzed studies involving adults diagnosed with ADHD (or showing clinically significant symptoms). They included:
They focused specifically on outcomes beyond symptoms:
The Results:
1. Strongest Effects: Occupational functioning
CBT showed consistently strong improvements in work-related functioning compared to control groups, both immediately after treatment and at follow-up. This was the most robust finding across domains.
2. Moderate Improvement: Global Functional Impairment
CBT led to moderate improvements in overall daily functioning, with some evidence that gains persist over time. In studies tracking individuals over time, improvements were even stronger at follow-up.
3. Modest Gains: Social Relationships
CBT produced small to moderate improvements in social functioning. Benefits were present both after treatment and at follow-up, but were less pronounced than in work-related outcomes.
4. Limited Effects: Academic Functioning
There were moderate short-term gains when CBT was compared to control groups, but these did not persist at follow-up. Within-subject studies showed only small improvements overall.
5. Modest and Inconsistent Effects: Quality of Life
Improvements in quality of life were small when compared to control groups and often did not last. However, studies tracking individuals over time showed moderate improvements, suggesting some benefit that may not always show up clearly in between-group comparisons.
Overall, the findings suggest:
One notable nuance: CBT did not always outperform other active treatments (like medication or other therapies). This suggests that while CBT is effective, its benefits may partly overlap with broader therapeutic or support effects rather than relying on a single, unique mechanism.
The Take-Away:
CBT is a valuable, evidence-based treatment for adults with ADHD, especially for improving work functioning and overall daily life management. However, its impact on relationships, academic outcomes, and quality of life is more limited and less consistent, pointing to the need for more targeted or combined approaches in those areas.
The Background:
ADHD and epilepsy are the two most common neurological disorders in children and adolescents. Additionally, they appear as co-diagnoses more often than chance would predict. Roughly a quarter of children with epilepsy also have ADHD, and children with ADHD face a 2.5-times greater risk of developing epilepsy than their peers.
Clinicians have long suspected that carrying both diagnoses compounds cognitive difficulties, but no rigorous quantitative review has mapped out exactly how much, or in what ways. This new meta-analysis now fills that gap.
The Study:
The team pooled data from peer-reviewed studies that included children and adolescents diagnosed with both conditions alongside at least one comparison group: children with neither condition, children with epilepsy alone, or children with ADHD alone. To capture the breadth of thinking skills, they constructed a general intelligence factor drawing on six cognitive domains:
The Results:
Across eleven studies (995 participants), children and adolescents with both conditions scored moderately lower on general intelligence than those with epilepsy alone. The same pattern held across all six cognitive domains. Seven studies (785 participants) comparing the dual-diagnosis group with those who had ADHD alone found an equally consistent moderate deficit, replicated in every domain.
The clearest signal emerged when researchers compared children and adolescents carrying both diagnoses to typically-developing peers. Seven studies covering 427 individuals revealed a substantially larger gap in general intelligence, with the effects of the two conditions appearing to be roughly additive, meaning the combined burden was approximately equal to the sum of each condition's individual impact. This pattern held across five of the six domains.
The Interpretation:
The results come with meaningful caveats. Variability across individual studies was moderate in the first two comparisons and high in the third, reflecting real differences in how studies were designed, which populations they sampled, and how they measured cognition. While there was no sign of publication bias in the first group, it was not assessed in two of the three analyses.
The authors describe “a widespread profile of cognitive dysfunction” in children and adolescents with both epilepsy and ADHD, while underscoring that the substantial variability between studies warrants caution in drawing overly precise conclusions. The findings nonetheless carry practical weight: children managing both conditions may need more intensive cognitive screening and support than current clinical practice routinely provides.
The focus on children and adolescents with ADHD often revolves around behavioral issues and academic difficulties, but the social struggles are real. Around 60% of youth with ADHD experience meaningful difficulties in social skills, reading social cues, and forming reciprocal relationships with peers. Over time, these struggles can raise the risk of anxiety and depression.
Medication remains the primary treatment for ADHD, with stimulants like methylphenidate (Ritalin) being the most commonly prescribed. While effective at reducing core symptoms such as inattention and impulsivity, medication has not been shown to improve social behavior or peer relationships.
The Background:
Exercise has recently emerged as a promising adjunctive therapy. A newly published meta-analysis examined whether structured physical activity can specifically improve social functioning in young people with ADHD. It builds on a previous review from 2015, addressing gaps that earlier work left open: social outcomes were rarely treated as a primary focus, and no prior analysis had systematically compared exercise types or asked how much exercise is actually needed to see benefits.
The Study:
The analysis included 13 randomized controlled trials involving 703 participants aged 6 to 18, all clinically diagnosed with ADHD. Only exercise programs lasting at least four weeks were considered. Studies that combined exercise with other therapies, such as psychotherapy, were excluded to isolate exercise's specific effects.
The researchers used a technique called network meta-analysis, which allows different interventions to be compared against one another even when they haven't been tested head-to-head, alongside dose-response modeling to identify how much exercise produces the greatest benefit.
Results:
The most striking results came from closed-skill exercise: across four studies involving 92 participants, it was associated with a very large reduction in social dysfunction. Open-skill exercise, by contrast, showed no measurable improvement across four studies with 91 participants. Multicomponent exercise (the group combining elements of both open- and closed-skill) reported large gains in two smaller studies with 33 participants.
Mind-body exercise showed a moderate benefit across three studies involving 44 participants.
The dose-response analysis offered a practically useful finding: 30 to 60 minutes of moderate-intensity exercise per day appeared to produce the best outcomes, with a minimum of roughly 15 to 30 minutes daily needed to achieve any meaningful benefit.
The Take-Away:
The results are encouraging but should be interpreted carefully. The number of studies in each category was small (two to three studies each), and sample sizes were modest, meaning the findings may not hold up as more evidence accumulates. The absence of publication bias is reassuring, as is the use of rigorous methodology, but this remains an early-stage evidence base. Larger, well-designed trials are needed before firm clinical recommendations can be made.
For now, the findings position structured physical activity (particularly closed-skill and multicomponent exercise) as a plausible complement to existing ADHD treatment, specifically targeting the social difficulties that medication tends not to address. The practical dose guidance is a useful starting point: around half an hour of moderate daily exercise as a minimum, with an hour as the apparent sweet spot. As low-risk additions to a treatment plan go, that’s a relatively accessible bar for most families to consider alongside professional guidance.
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