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April 7, 2021
There is a growing interest (and controversy) in 'adult-onset ADHD. No current diagnostic system allows for the diagnosis of ADHD in adulthood, yet clinicians sometimes face adults who meet all criteria for ADHD, except for age at onset. Although many of these clinically referred adult-onset cases may reflect poor recall, several recent longitudinal population studies have claimed to detect cases of adult-onset ADHD that showed no signs of ADHD as a youth (Agnew-Blais, Polanczyk et al. 2016, Caye, Rocha, et al. 2016). They conclude, not only that ADHD can onset in adulthood, but that childhood-onset and adult-onset ADHD may be distinct syndromes(Moffitt, Houts, et al. 2015)
In each study, the prevalence of adult-onset ADHD was much larger than the prevalence of childhood-onset adult ADHD). These estimates should be viewed with caution. The adults in two of the studies were 18-19 years old. That is too small a slice of adulthood to draw firm conclusions. As discussed elsewhere (Faraone and Biederman 2016), the claims for adult-onset ADHD are all based on population as opposed to clinical studies.
Population studies are plagued by the "false positive paradox", which states that, even when false positive rates are low, many or even most diagnoses in a population study can be false.
Another problem is that the false positive rate is sensitive to the method of diagnosis. The child diagnoses in the studies claiming the existence of adult-onset ADHDused reports from parents and/or teachers but the adult diagnoses were based on self-report. Self-reports of ADHD in adults are less reliable than informant reports, which raises concerns about measurement error. Another longitudinal study found that current symptoms of ADHD were under-reported by adults who had had ADHD in childhood and over-reported by adults who did not have ADHD in childhood(Sibley, Pelham, et al. 2012). These issues strongly suggest that the studies claiming the existence of adult-onset ADHD underestimated the prevalence of persistent ADHD and overestimated the prevalence of adult-onset ADHD. Thus, we cannot yet accept the conclusion that most adults referred to clinicians with ADHD symptoms will not have a history of ADHD in youth.
The new papers conclude that child and adult ADHD are "distinct syndromes", "that adult ADHD is more complex than a straightforward continuation of the childhood disorder" and that adult ADHD is "not a neurodevelopmental disorder". These conclusions are provocative, suggesting a paradigm shift in how we view adulthood and childhood ADHD. Yet they seem premature. In these studies, people were categorized as adult-onset ADHD if full-threshold add had not been diagnosed in childhood. Yet, in all of these population studies, there was substantial evidence that the adult-onset cases were not neurotypical in adulthood (Faraone and Biederman 2016). Notably, in a study of referred cases, one-third of late adolescent and adult-onset cases had childhood histories of ODD, CD, and school failure(Chandra, Biederman, et al. 2016). Thus, many of the "adult onsets" of ADHD appear to have had neurodevelopmental roots.
Looking through a more parsimonious lens, Faraone and Biederman(2016)proposed that the putative cases of adult-onset ADHD reflect the existence of subthreshold childhood ADHD that emerges with full threshold diagnostic criteria in adulthood. Other work shows that subthreshold ADHD in childhood predicts onsets of full-threshold ADHD in adolescence(Lecendreux, Konofal, et al. 2015). Why is onset delayed in subthreshold cases? One possibility is that intellectual and social supports help subthreshold ADHD youth compensate in early life, with decompensation occurring when supports are removed in adulthood or the challenges of life increase. A related possibility is that the subthreshold cases are at the lower end of a dimensional liability spectrum that indexes risk for onset of ADHD symptoms and impairments. This is consistent with the idea that ADHD is an extreme form of a dimensional trait, which is supported by twin and molecular genetic studies(Larsson, Anckarsater, et al. 2012, Lee, Ripke, et al. 2013). These data suggest that disorders emerge when risk factors accumulate over time to exceed a threshold. Those with lower levels of risk at birth will take longer to accumulate sufficient risk factors and longer to onset.
In conclusion, it is premature to accept the idea that there exists an adult-onset form of ADHD that does not have its roots in neurodevelopment and is not expressed in childhood. It is, however, the right time to carefully study apparent cases of adult-onset ADHD to test the idea that they are late manifestations of a subthreshold childhood condition.
Agnew-Blais, J. C., G.V. Polanczyk, A. Danese, J. Wertz, T. E. Moffitt and L. Arseneault (2016)."Persistence, Remission and Emergence of ADHD in Young Adulthood:Resultsfrom a Longitudinal, Prospective Population-Based Cohort." JAMA.Caye, A., T. B.-M. Rocha, L. Luciana Anselmi, J. Murray, A. M.B. Menezes, F. C. Barros, H. Gonçalves, F. Wehrmeister, C. M. Jensen, H.-C.Steinhausen, J. M. Swanson, C. Kieling and L. A. Rohde (2016). "ADHD doesnot always begin in childhood: E 1 vidence from a large birth cohort." JAMA.
Chandra, S., J. Biederman and S. V. Faraone (2016)."Assessing the Validity of the Ageat Onset Criterion for Diagnosing ADHD in DSM-5." J Atten Disord.
Faraone, S. V. and J. Biederman (2016). "CanAttention-Deficit/Hyperactivity Disorder Onset Occur in Adulthood?" JAMAPsychiatry.
Larsson, H., H. Anckarsater, M. Rastam, Z. Chang and P.Lichtenstein (2012). "Childhood attention-deficit hyperactivity disorderas an extreme of a continuous trait: a quantitative genetic study of 8,500 twinpairs." J Child Psychol Psychiatry53(1): 73-80.
Lecendreux, M., E. Konofal, S. Cortese and S. V. Faraone(2015). "A 4-year follow-up of attention-deficit/hyperactivity disorder ina population sample." J Clin Psychiatry76(6): 712-719.
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Sibley, M. H., W. E. Pelham, B.S. Molina, E. M. Gnagy, J. G. Waxmonsky, D. A. Waschbusch, K. J. Derefinko, B.T. Wymbs, A. C. Garefino, D. E. Babinski and A. B. Kuriyan (2012). "Whendiagnosing ADHD in young adults emphasize informant reports, DSM items, and impairment."J Consult Clin Psychol80(6):1052-1061.
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.
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.
Children and adolescents with ADHD come into contact with child welfare services (CWS) far more often than their peers. There are many contributing factors to consider, including the fact that hyperactivity and impulsivity frequently lead to behaviors that are considered disruptive and cause academic and social difficulties. Many of these children are also growing up in households marked by parental conflict and/or single-parent arrangements. All of these circumstances can compound vulnerability and, historically, increase the likelihood of CWS involvement.
Background:
In Norway, Child Welfare Services operate at the municipal level and are legally required in every local authority. Their scope spans investigation, family support, and, where necessary, out-of-home placement and ongoing monitoring. Grounds for intervention include abuse, neglect, behavioral or psychosocial difficulties, and inadequate care-giving. Norwegian CWS works closely with health, education, and social services and places a strong emphasis on keeping families together. Compared with systems in countries such as the United States, Poland, Romania, and the Czech Republic, the Norwegian approach sets a lower bar for intervention and leans toward home-based support, while setting a higher bar for out-of-home placements. This model is shared by other Nordic countries, as well as Germany and the United Kingdom.
Research into whether ADHD medication affects child welfare caseloads is remarkably sparse. A single Danish study previously found that medication treatment accounted for much of an observed decline in foster care cases, but no study had examined medication’s broader impact on CWS involvement, covering both supportive interventions and out-of-home placements.
Norway’s universal single-payer health system and comprehensive national registers make population-wide research of this kind feasible. Drawing on these resources, a Norwegian research team set out to test whether ADHD medication reduces children’s contact with CWS and their need for out-of-home placement.
The Study:
This study included all 5,930 children and adolescents aged 5 to 14 who received a clinical ADHD diagnosis from Child and Adolescent Mental Health Services between 2009 and 2011. Each was followed for up to 4 years post-diagnosis, the upper age limit being 18, at which point CWS jurisdiction ends. This group was compared with more than 53,000 peers who had no CWS contact during the same period.
The results showed a meaningful, though not dramatic, association between medication and reduced CWS contact. At one year, treated children had approximately 7% fewer contacts with CWS; by two years, that figure had risen to around 12%. The effect then narrowed, settling at roughly 7–8% reductions at the three- and four-year marks.
The picture for out-of-home placements is considerably less convincing. The research team highlighted a 3% reduction at two-year follow-up, but this finding barely crossed the threshold of statistical significance, and no effect was observed at the one-, three-, or four-year follow-up points.
The Take-Away:
The authors concluded that pharmacological treatment for ADHD is associated with reductions in both supportive CWS services and out-of-home placements among children affected by clinicians’ prescribing decisions in Norway. A more cautious reading of the same data, however, would emphasize an overall reduction in CWS contact of roughly 8%, while treating the out-of-home placement finding as, at best, inconclusive.
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