One of the most important challenges facing ADHD diagnosis today is that the population being identified with ADHD is not the same population that was being diagnosed 20 or 30 years ago. A recent study by LaBianca and colleagues, Changes in Genetic Contributions to ASD and ADHD by Year of Diagnosis, discusses reasons for this shift. By examining more than 20,000 individuals with ADHD in a large Danish cohort, the researchers found that those diagnosed in more recent years had, on average, lower genetic liability for ADHD than those diagnosed in earlier years. Similar patterns were found for autism spectrum disorder.
This finding does not mean that ADHD has become less genetic. Rather, it suggests that the population receiving an ADHD diagnosis has broadened. Historically, diagnosis may have disproportionately captured individuals with more pronounced genetic liability and more obvious, pervasive symptoms. As awareness has increased and diagnostic practices have expanded, people with less significant genetic risk — and potentially more subtle presentations, and presentations that may only occur in a particular context — are increasingly being identified. In ways, we can think of this as a shift toward the way that anxiety or depression is diagnosed. You don’t have to have suicidal thinking, or be unable to get out of bed in the morning to receive a diagnosis of depression. You don’t have to have a panic attack to be treated for anxiety. In other words, in the past, we only diagnosed more extreme cases of ADHD, leaving the rest to fend for themselves. Now, we realize that ADHD exists along a continuum and that less impacted individuals still benefit from diagnosis and treatment.
The growing prevalence of ADHD should not automatically be interpreted as evidence of overdiagnosis. It may, at least in part, reflect diagnostic expansion: the recognition of individuals who were always on the ADHD spectrum, but whose difficulties were previously overlooked, misunderstood, compensated for, or attributed to other causes.
This has profound implications for how we think about diagnosis. ADHD is a highly polygenic, dimensional neurodevelopmental condition. Genetic liability exists along a continuum rather than dividing neatly into “ADHD” and “not ADHD.” Yet our diagnostic system asks clinicians to make a categorical determination based largely on whether an individual endorses a specified number of symptoms, whether those symptoms were present during childhood, and whether they occur across more than one setting.
A symptom checklist cannot adequately capture the complexity of this continuum.
Two individuals may have similar underlying vulnerabilities but look remarkably different clinically. One may be hyperactive and impulsive and have struggled academically and socially since childhood. Another may be predominantly inattentive, highly intelligent, and successful in school or work because of extraordinary compensatory strategies — until increasing demands, parenthood, menopause, a career transition, or other life changes overwhelm those strategies. Both may have significant ADHD-related impairment, but only one may resemble the traditional clinical picture that shaped our diagnostic criteria.
The changing genetic profile of those receiving ADHD diagnoses reinforces the need to move beyond a narrow checklist-based approach. The question should not simply be, “Does this person have enough symptoms to qualify for ADHD?” A more clinically meaningful question is: “Does this person demonstrate a persistent pattern of neurodevelopmental difficulties consistent with ADHD that meaningfully interferes with functioning, and does ADHD provide the best explanation for those difficulties?”
This requires assessment of executive functioning, emotional regulation, motivation, time management, self-regulation, working memory, sleep, sensory and environmental demands, compensatory strategies, and the individual’s developmental and functional history. It also requires attention to when and where difficulties emerge and why they may become more apparent at particular points in the lifespan. The more intelligent or talented an individual is, the greater the environmental demand is required before ADHD patterns are manifested. It’s an interaction between the individual’s brain, taking into account many traits other than ADHD, and the demands of the environment in which they are trying to function.
The LaBianca study therefore offers an important lesson: as our recognition of ADHD expands, the population we diagnose becomes increasingly heterogeneous. Our diagnostic model must expand with it. Even within a single individual, they may appear to “have” ADHD at one point in their life and to “not have” ADHD at another point because of multiple factors including compensatory abilities and environmental demands.
ADHD diagnosis should not be abandoned; it should be made more clinically sophisticated. The goal is not to diagnose more people indiscriminately, but to identify ADHD more accurately — across genders, ages, settings, levels of ability, and stages of life. A modern approach must recognize ADHD as a dimensional condition whose expression and functional consequences can change over time.
The challenge for the next generation of ADHD care is not simply to diagnose more people. It is to diagnose people at all levels of accomplishment — and to understand them more completely.
Reference
LaBianca, S., Lousdal, M. L., Krebs, M. D., et al. (2026). Changes in genetic contributions to ASD and ADHD by year of diagnosis. JAMA Psychiatry. Advance online publication. https://doi.org/10.1001/jamapsychiatry.2026.1247