Why are females less likely to be diagnosed with ADHD in childhood than males?

This article describes a comprehensive meta-analysis that was conducted to estimate the prevalence of attention-deficit/hyperactivity disorder (ADHD), as defined by the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV). A systematic literature review identified 86 studies of children and adolescents (N = 163,688 individuals) and 11 studies of adults (N = 14,112 individuals) that met inclusion criteria for the meta-analysis, more than half of which were published after the only previous meta-analysis of the prevalence of ADHD was completed. Although prevalence estimates reported by individual studies varied widely, pooled results suggest that the prevalence of DSM-IV ADHD is similar, whether ADHD is defined by parent ratings, teacher ratings, or a best estimate diagnostic procedure in children and adolescents (5.9-7.1 %), or by self-report measures in young adults (5.0 %). Analyses of diagnostic subtypes indicated that the predominantly inattentive type is the most common subtype in the population, but individuals with the combined type are more likely to be referred for clinical services. Additional research is needed to determine the etiology of the higher prevalence of ADHD in males than females and to clarify whether the prevalence of ADHD varies as a function of socioeconomic status or ethnicity. Finally, there were no significant prevalent differences between countries or regions of the world after controlling for differences in the diagnostic algorithms used to define ADHD. These results provide important support for the diagnostic validity of ADHD, and argue against the hypothesis that ADHD is a cultural construct that is restricted to the United States or any other specific culture.

Attention-deficit/hyperactivity disorder (ADHD) is a persistent neurodevelopmental disorder that affects 5% of children and adolescents and 2.5% of adults worldwide. Throughout an individual's lifetime, ADHD can increase the risk of other psychiatric disorders, educational and occupational failure, accidents, criminality, social disability and addictions. No single risk factor is necessary or sufficient to cause ADHD. In most cases ADHD arises from several genetic and environmental risk factors that each have a small individual effect and act together to increase susceptibility. The multifactorial causation of ADHD is consistent with the heterogeneity of the disorder, which is shown by its extensive psychiatric co-morbidity, its multiple domains of neurocognitive impairment and the wide range of structural and functional brain anomalies associated with it. The diagnosis of ADHD is reliable and valid when evaluated with standard criteria for psychiatric disorders. Rating scales and clinical interviews facilitate diagnosis and aid screening. The expression of symptoms varies as a function of patient developmental stage and social and academic contexts. Although there are no curative treatments for ADHD, evidenced-based treatments can markedly reduce its symptoms and associated impairments. For example, medications are efficacious and normally well tolerated, and various non-pharmacological approaches are also valuable. Ongoing clinical and neurobiological research holds the promise of advancing diagnostic and therapeutic approaches to ADHD. For an illustrated summary of this Primer, visit: http://go.nature.com/J6jiwl.

Decades of research show that genes play an vital role in the etiology of attention deficit hyperactivity disorder (ADHD) and its comorbidity with other disorders. Family, twin, and adoption studies show that ADHD runs in families. ADHD’s high heritability of 74% motivated the search for ADHD susceptibility genes. Genetic linkage studies show that the effects of DNA risk variants on ADHD must, individually, be very small. Genome-wide association studies (GWAS) have implicated several genetic loci at the genome-wide level of statistical significance. These studies also show that about a third of ADHD’s heritability is due to a polygenic component comprising many common variants each having small effects. From studies of copy number variants we have also learned that the rare insertions or deletions account for part of ADHD’s heritability. These findings have implicated new biological pathways that may eventually have implications for treatment development.