November 10, 2023

How do psychiatric comorbidities affect risk of premature death among children and adults with ADHD?

The Nordic countries maintain detailed registers of their inhabitants. This enables researchers to examine patterns over entire nations. An international research team used the Swedish national registers for a prospective cohort study of 2,675,615 persons in the Medical Birth Register born in Sweden over a 27-year period from January 1, 1983, through December 31, 2009. Follow-up was completed in December 2013, with the oldest cohort member aged 31. The mean age at study entry was 6, and the mean at follow-up was 11.

Using personal identification numbers, researchers were able to cross-reference with the National Patient Register and the National Drug Register. From this, they determined that 86,670 members of the cohort (3.2 percent) had ADHD, based either on records of clinical diagnosis or of prescription of ADHD drugs. Psychiatric comorbidities were likewise identified in the National Patient Register.

These comorbidities were significantly more prevalent in the ADHD population than in the rest of the cohort. For example, whereas only 2.2% of the non-ADHD group was diagnosed with substance use disorder (SUD), 13.3% of the ADHD group also had SUD, a six-fold difference. For depression, it was a seven-fold difference, for schizophrenia a nine-fold difference.

The ADHD group had a significantly higher risk of premature death from all causes than the non-ADHD group, with an adjusted hazard ratio (HR) of 3.94 (95% CI 3.51-4.43). Unintentional injury(36%) and suicide (31%) were the leading causes of death in the ADHD group. Those with ADHD were more than eight times more likely to die by suicide than non-ADHD individuals, and roughly four times more likely to die from unintentional injury.

The vast majority of the increased risk appears to be associated with comorbid psychiatric conditions. Those with ADHD but no diagnosed comorbidities had an adjusted HR of 1.41 (95% CI 1.01-1.97). With a single comorbidity, the HR more than doubled to 3.71 (95% CI 2.88-4.78). With four or more comorbidities, it rose to a staggering 25.22 (95% CI 19.6-32.46).

The comorbid condition with the greatest impact was SUD, which increased the risk eight-fold by comparison with those with only ADHD (HR = 8.01, 95% CI 6.16-10.41). Anxiety disorder, schizophrenia, and personality disorder increased the risk about fourfold. Bipolar disorder, depression, and eating disorder increased risk by roughly two and a half times.

Co variate analysis helped tease out what portion of the risk was associated with ADHD alone versus comorbid conditions. Adjusting for the year of birth, sex, birth weight, maternal age at birth, parental educational level, and parental employment status, those with ADHD (including comorbid conditions) were 2.7 times more likely to prematurely die of natural causes than those without. Adjusting for comorbid psychiatric conditions completely eliminated the risk from ADHD alone (HR = 1.01, 95% CI .72-1.42).

Likewise, those with ADHD (including comorbid conditions) were six times as likely to die of unnatural causes. Adjusting for early-onset comorbid disorders(such as conduct disorders, autism spectrum disorder, and intellectual disability) only modestly reduced the HR to 5.3, but further adjusting for later-onset comorbid disorders (including substance use disorder, depressive disorder, bipolar disorder, anxiety disorder, schizophrenia, personality disorder, and eating disorders) reduced the HR to 1.57 (95% CI 1.35-1.83), and reduced it to insignificance in the case of suicide (HR = 1.13, 95% CI.88-1.45).

Summing up, the lion’s share of the greater risk of premature death in persons with ADHD is attributable to psychiatric comorbidities. Nevertheless, those with ADHD alone still face a 40 percent greater risk than those without ADHD.

The study did not examine effects of ADHD medication, which the authors state “should be analyzed because of documented potential benefits on ADHD symptoms and comorbid disorders.”

The authors concluded, “Among adults, early-onset psychiatric comorbidity contributed substantially to the premature mortality risks due to natural causes. On the other hand, later-onset psychiatric comorbidity, especially SUD, explained a substantial part of the risk for unnatural deaths, including all the risk of suicide deaths and most of the deaths due to unintentional injuries. These results suggest that overall health conditions and risk of psychiatric comorbidity should be evaluated clinically to identify high-risk groups among individuals with ADHD.”

Shihua Sun, MD; Ralf Kuja-Halkola, Ph.D.; Stephen V. Faraone, Ph.D.; Brian M. D’Onofrio, Ph.D.; Søren Dalsgaard, Ph.D.; ZhengChang, Ph.D.; Henrik Larsson, Ph.D., “Association of Psychiatric Comorbidity With the Risk of Premature Death Among Children and Adults With Attention-Deficit/Hyperactivity Disorder,” JAMA Psychiatry doi:10.1001/jamapsychiatry.2019.1944Published online August 7, 2019.

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Exercise as an ADHD Intervention: What Two Recent Meta-Analyses Tell Us

Exercise has attracted growing attention as an intervention for ADHD. As a potential treatment option for ADHD, it is, of course, highly appealing because it can be low- to no-cost, widely accessible, and free of the side effects that can accompany medication. From previous studies, we know that certain types of exercise may be more effective than others, but do we actually know enough for clinicians to prescribe physical activity as a treatment for ADHD? 

The First Study: Effects on Core ADHD Symptoms 

Despite encouraging findings in individual studies, researchers have lacked clear guidance on which types of exercise work best, at what intensity, and for how long. A meta-analysis by Chen et al. set out to address this by pooling data from 20 randomized controlled trials (RCTs) involving 841 children and adolescents aged 4–18, all of which compared exercise interventions against non-exercising control groups. 

The results were cautiously optimistic. Across standardized symptom scales, exercise produced a small improvement in ADHD symptoms overall. Objective cognitive tests showed a moderate improvement. Emotional and behavioral outcomes, however, showed no significant change. 

To understand what was driving differences between studies, the researchers broke results down by exercise type. Therapeutic and alternative exercises (targeted movements and specific techniques such as those prescribed by physical therapists) were associated with moderate symptom improvements. Mind-body practices (such as yoga or tai chi) showed small-to-moderate gains. Conventional aerobic exercise yielded smaller effects, while skill-based competitive sports showed no measurable benefit. Notably, the variability between individual studies remained high throughout, meaning these categories should be interpreted with some caution. 

Results:

The authors recommend that clinicians and parents consider incorporating therapeutic or alternative exercise sessions twice a week, each lasting 60–90 minutes, as a supplemental strategy alongside existing ADHD treatment. They stop short of calling this definitive, noting that future research should clarify how exercise produces its effects and how it might best be combined with medication or behavioral therapy. 

The Second Study: Effects on Inhibitory Control 

A second meta-analysis, by Zhang et al., zoomed in on a specific and particularly relevant cognitive challenge in ADHD: inhibitory control. Inhibitory control refers to the ability to suppress impulsive responses and tune out irrelevant distractions. This capacity underlies much of the restlessness, interrupting, and difficulty staying on task that characterize the condition. 

This analysis drew on 34 studies with over 1,300 participants spanning all age groups, making it broader in scope than the Chen et al. review. Overall, exercise was associated with a moderate improvement in inhibitory control. When the analysis was restricted to RCTs alone, this finding held up. When studies with a high risk of bias were excluded, however, the effect size dropped to small-to-moderate. 

One notable null result: three studies that used EEG to measure brain activity during inhibitory tasks found no significant effects on the neural signatures most closely tied to this process. This suggests exercise may influence behavior without necessarily changing the underlying brain mechanisms researchers expected, or that current methods aren't yet sensitive enough to detect such changes. 

The dosing question produced some of the more practically useful findings. Single exercise sessions yielded only borderline small improvements. Sustained exercise programs, by contrast, showed moderate improvements, and programs with sessions three times per week produced large gains and had the strongest effect between the two meta-analyses. Exercise intensity and total program duration, perhaps interestingly, were not significant factors. 

Results: 

The authors are measured in their conclusions: exercise shows a real but modest benefit for inhibitory control, and frequency appears to matter more than intensity. They caution against overstating the case for exercise as treatment for ADHD overall, as it did not significantly affect hyperactivity or impulsivity as standalone outcomes, and its neural effects remain unclear. 

The Broader Picture

Ultimately, these two meta-analyses support exercise as a meaningful supplemental intervention for ADHD, particularly for attention and cognitive control, while urging realistic expectations. Neither suggests exercise should replace established treatments. Both are limited by high variability across the underlying studies, and both call for better-designed research to sharpen the guidance available to clinicians and families. 

 

 

 

The Neurocognitive Roots of Boredom in ADHD: a Meta-Analysis

Boredom is more than just feeling restless or under-stimulated. It’s a negative emotional state that arises when activities feel meaningless or dull and, for those with ADHD, this negative emotional state might be markedly more intense. Researchers increasingly view boredom as functional: an internal signal pushing people to seek more rewarding and meaningful experiences. But for some, that signal becomes chronic and overwhelming.

People who are highly prone to boredom face a range of psychological and behavioral consequences, including anxiety, depression, difficulty identifying their own emotions (alexithymia), impulsivity, and physical complaints. These struggles often surface in harmful behaviors: overeating, substance use, compulsive internet use, and gambling.

For people with ADHD, boredom can cross into genuine distress. Many describe it as “torture” or “an itchy coat you can’t scratch”,  language that conveys not mild discomfort but an urgent, almost unbearable need to escape. This makes sense given that ADHD involves core difficulties with attention, arousal regulation, and motivation, all of which make sustained engagement harder and boredom far more likely.

The Study:

A recent meta-analysis of 18 studies involving more than 22,000 participants confirmed a moderately strong and consistent positive association (an overall effect size of r = 0.40) between ADHD and self-reported boredom. All but one study found significant results, and there was no evidence of publication bias.

“While the relationship between ADHD and boredom may seem obvious,” the authors state, “this has paradoxically led to the phenomenon being understudied.”

Despite how significant this connection appears to be, the researchers noted it has attracted surprisingly little scientific attention; a gap they attribute to a widespread assumption that boredom in ADHD is simply a byproduct of inattention or impulsivity, and therefore not worth studying on its own terms. They push back on that view, arguing that boredom may be a more fundamental part of the ADHD experience: a bridge between atypical brain function and the behavioral, emotional, and cognitive difficulties that shape long-term outcomes.

The Take-Away: 

Ultimately, addressing the profound boredom experienced by individuals with ADHD requires a multifaceted approach that goes beyond simply treating inattention. Researchers emphasize the need for rigorous studies to determine if stimulant medications actively reduce this intense boredom by repairing underlying brain mechanisms, rather than just as a side effect of improved focus. Beyond medication, tailored psychological therapies may offer promise; psychoeducation can help individuals reframe boredom as a biological signal rather than a personal failure or character flaw. 

Additionally, another approach suggests that rather than solely focusing on treating the individual, systemic issues must be addressed, such as the effects of low-stimulation environments. For example, prioritizing a better "person-environment fit" through smaller class sizes, flexible academic pacing, and/or offering highly stimulating, novel tasks, schools and workplaces can offer meaningful relief from the chronic distress of ADHD-related boredom. 

May 11, 2026

Early Skull Fusion in Infants Linked to Higher ADHD Risk

A new study from Japan suggests that infants born with craniosynostosis are significantly more likely to be diagnosed with ADHD later in childhood. Craniosynostosis is a condition in which the bony plates of the skull fuse prematurely, leading to increased intracranial pressure. 

The Background:

Craniosynostosis affects roughly one in every 2,000 births. When the skull’s natural seams close prematurely, it can restrict brain growth and increase intracranial pressure, potentially reducing blood flow to the brain. Because the condition is relatively rare, it has been difficult to study at scale until now. 

The Study:

To overcome this, researchers tapped into a large Japanese insurance database compiled by JMDC, Inc., which holds records on around 20 million people, or about 15% of Japan’s population. Drawing on two decades of data, the team tracked over 338,000 mother-child pairs. Children with related genetic syndromes or chromosomal conditions such as Down syndrome were excluded to keep the focus on craniosynostosis itself. 

Of the children studied, around 1,145 had craniosynostosis, and 7,325 were diagnosed with ADHD. After accounting for factors like sex, birth year, maternal age, mental health history, pregnancy infections, and birth complications, children with craniosynostosis were found to have roughly 2.4 times the risk of a subsequent ADHD diagnosis compared to those without it. 

To test whether shared family genetics or home environment might be driving the association rather than the skull condition itself, the researchers conducted a separate analysis among siblings. The elevated risk remained at 2.2 times. The consistency of the finding across both analyses strengthens the case for a genuine biological link. 

The Results:

The results point to raised intracranial pressure and restricted cerebral blood flow as plausible mechanisms, though the study’s observational design means causation cannot be confirmed. Ultimately, these findings highlight the need for proactive, long-term care strategies for those born with craniosynostosis. By establishing a solid link between premature skull fusion and a significantly higher risk of ADHD, the research demonstrates that medical care for this condition should not end once the skull's physical structure is addressed.

The Takeaway:

Pediatricians, neurologists, and parents can use this data to implement early, routine behavioral and developmental screening for these children as they grow. This additional support would ensure that those who do develop ADHD can receive timely interventions, educational aids, and therapies, ultimately improving their long-term developmental outcomes.