The researchers studied a birth cohort of 1,037 individuals born in Dunedin, New Zealand, in 1972 and 1973 and followed them to age 38. A number of factors were assessed, including symptoms of ADHD, associated clinical features, comorbid disorders, neuropsychological deficits, genomewide association study-derived polygenic risk, and life impairment indicators. Adult ADHD diagnoses used DSM-5 criteria.
As the researchers had expected, childhood ADHD had a prevalence of 6% (predominantly male) and was associated with childhood comorbid disorders, neurocognitive deficits, polygenic risk, and residual adult life impairment. Also as expected, adult ADHD had a prevalence of 3% (gender balanced) and was associated with adult substance dependence, adult life impairment, and treatment contact. However, the researchers were surprised to find that 90% of adult ADHD cases lacked a history of childhood ADHD. Another unexpected finding was that the adult ADHD group did not show tested neuropsychological deficits in childhood or adulthood, nor did they show polygenic risk for childhood ADHD.
The researchers concluded that if the study findings are replicated, the disorder’s place in the classification system as a neurodevelopment disorder manifesting early in development needs to be reconsidered and that research should be conducted on the etiology of adult ADHD.
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