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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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Moffitt, T. E., R. Houts, P. Asherson, D. W. Belsky, D. L.Corcoran, M. Hammerle, H. Harrington, S. Hogan, M. H. Meier, G. V. Polanczyk,R. Poulton, S. Ramrakha, K. Sugden, B. Williams, L. A. Rohde and A. Caspi(2015). "Is Adult ADHD a Childhood-Onset Neurodevelopmental Disorder?Evidence From a Four-Decade Longitudinal Cohort Study." Am J Psychiatry:appiajp201514101266.
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.
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.
Stimulant medications, such as methylphenidate (Ritalin) and amphetamines (Adderall), are among the most widely prescribed drugs in the world. In the United States alone, prescription rates have climbed more than 50% over the past decade, driven largely by growing awareness of ADHD in both children and adults. Yet stimulants also have a long history of non-medical use, and concerns about their psychological risks persist among patients, families, and clinicians alike.
Two major studies now offer the clearest picture yet of what that risk actually looks like, and who it may affect.
The Background:
Before turning to the research, it helps to understand the landscape. A notable share of stimulant users misuse their medication: roughly one in four takes it in ways other than prescribed, and about one in eleven meets criteria for Prescription Stimulant Use Disorder (PSUD). Counterintuitively, most people with PSUD aren’t obtaining drugs illicitly — they’re misusing their own prescriptions.
This distinction between therapeutic and non-therapeutic use turns out to be critical when evaluating psychosis risk.
The Study:
A comprehensive meta-analysis by Jangra and colleagues pooled data across more than a dozen studies to compare psychotic outcomes in people using stimulants therapeutically versus non-therapeutically. The contrast was striking.
Among therapeutic users (more than 220,000 individuals taking stimulants at prescribed doses under medical supervision), psychotic episodes occurred in roughly one in five hundred people. When symptoms did appear, they typically emerged after prolonged treatment or in individuals with pre-existing psychiatric vulnerabilities, and they usually resolved when the medication was stopped.
Among non-therapeutic users (over 8,000 participants across twelve studies, many using methamphetamine or high-dose amphetamines), nearly one in three experienced psychotic symptoms. These episodes tended to be more severe, involving persecutory delusions and hallucinations, with faster onset and a greater likelihood of recurrence or persistence.
The biology underlying this difference is well understood. When stimulants are taken orally at guideline-recommended doses, they produce moderate, gradual changes in neurotransmitter activity central to attention and executive functions. The brain tolerates these changes relatively well. Non-therapeutic use, by contrast, often involves much higher doses that are frequently delivered through non-oral routes such as injection or smoking. This produces a rapid, excessive surge in dopamine activity, which is precisely the neurochemical pattern associated with psychotic symptoms.
The takeaway here is not that therapeutic stimulant use is risk-free, but that risk is strongly modulated by dose, route of administration, and individual psychiatric history. Clinicians are advised to monitor patients with pre-existing mood or psychotic disorders, particularly carefully.
A Nationwide Study Focuses on Methylphenidate Specifically:
Where the meta-analysis cast a wide net, a large-scale population study by Healy and colleagues drilled into a specific and clinically pressing question: does methylphenidate (the most commonly prescribed ADHD medication, also known as Ritalin) increase the risk of developing a psychotic disorder?
To find out, the researchers analyzed Finland's national health insurance database, tracking nearly 700,000 individuals diagnosed with ADHD. Finland's single-payer system made this kind of comprehensive, long-term tracking possible in a way that fragmented healthcare systems rarely allow.
Critically, the team adjusted for a range of confounding factors that have clouded previous research, including sex, parental education, parental history of psychosis, and the number of psychiatric visits and diagnoses prior to the ADHD diagnosis itself (a proxy for illness severity). After these adjustments, they found no significant difference in the risk of schizophrenia or non-affective psychosis between patients treated with methylphenidate and those who remained unmedicated. This held true even among patients with four or more years of continuous methylphenidate use.
The Take-Away:
When considered together, these studies offer meaningful reassurance without encouraging complacency.
For patients and families weighing ADHD treatment, the evidence suggests that methylphenidate used as prescribed does not increase psychosis risk, even over years of use. The rare cases of stimulant-associated psychosis in therapeutic settings are typically linked to high doses, pre-existing vulnerabilities, or both, and tend to resolve with discontinuation.
For clinicians, the findings reinforce the importance of baseline psychiatric assessment before initiating stimulant therapy, ongoing monitoring in patients with mood or psychotic disorder histories, and clear patient education about the risks of dose escalation or non-oral use.
The picture that emerges is one of a meaningful distinction between a medication used carefully within its therapeutic window and a drug misused outside of it. This distinction matters enormously when communicating risk to patients, policymakers, and the public.
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