Persistence and emergence of ADHD in young adulthood: Unravelling aetiology using genetics in a population-based longitudinal cohort

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While ADHD was historically thought to only affect children, it is now recognized that it may continue into adulthood. Studies identify about 2.5-5% of adults as having ADHD, which is associated with poor outcomes including unemployment, substance abuse, and even higher mortality. I recently conducted a study that found not only may ADHD continue into adulthood, but the disorder may also newly begin in young adulthood. This is a novel finding, as ADHD is currently understood to begin in childhood. My findings are supported by results from two other recent studies in Brazil and New Zealand that also identified late-onset ADHD groups. Currently, little is known about those adults who did not have ADHD in childhood but developed it in adulthood. Who are individuals with late-onset ADHD? Did they have a disposition to develop ADHD as children, but grew up in very supportive households that masked their disorder until later life? Or do these people not have ADHD in adulthood, but rather another disorder with symptoms that could look like ADHD?Genetic studies can provide crucial insights in answering such questions about late-onset ADHD, and indeed broader questions about ADHD in young adulthood. One way to understand how late-onset ADHD might be similar or different to childhood ADHD is to investigate whether people with late-onset ADHD have higher levels of risk genes for childhood ADHD. If so, this would support the idea that people with late-onset ADHD would have shown ADHD in childhood, but the disorder was perhaps masked by a supportive family environment. In contrast, if people with late-onset ADHD do not have more risk genes for ADHD, but rather for other mental health disorders, this would suggest that late-onset ADHD may be explained by other mental health problems with symptoms similar to ADHD.The age at which ADHD symptoms may appear varies broadly from person to person, with some individual's symptoms beginning in infancy, while for others symptoms may not emerge until adolescence or later. I will examine how genes affect whether an individual develops either childhood or adult-onset ADHD, as well as how genes affect when ADHD symptoms first begin across a range of ages over development. It is not known whether some genes may increase risk for a very early onset of ADHD (e.g. infancy) whereas others increase risk for later onset (i.e. late childhood), and whether genes that affect when ADHD begins are different from those that affect whether an individual develops ADHD in the first place. Genes do not act alone to increase risk for ADHD. Rather, people's genes interact with their environment to influence the development of ADHD. For example, even people with many ADHD risk genes may not develop the disorder if they grow up in a protective environment; likewise, people with few ADHD risk genes might develop the disorder if they grow up in adverse environments. I will explore aspects of the social and family environment that could protect against or exacerbate genetic risk for ADHD. One pathway through which the environment can influence risk of ADHD is through epigenetics changes, which can turn genes 'on and off'. In this way, two identical twins who share 100% of their DNA may express different genes depending on epigenetic variations. I will compare epigenetic differences among twin pairs in which one twin has late-onset ADHD and the other does not, to identify biological changes that may be markers of young adult ADHD. To-date, the majority of ADHD research has assumed that all cases of adult ADHD began in childhood. However, I and other researchers have recently found this may often not be the case. Understanding how, why and when adult ADHD may develop is a crucial question and has broad implications for the diagnosis and treatment of adult ADHD.