ebook_ADHD2019

4 Rohde, Buitelaar, Gerlach & Faraone at onset of ADHD and for variability in the persistence of the disorder into adul- thood. For a review of the genetics of adult ADHD, see Franke et al. 6 As reviewed by Faraone and Larsson, 4 family and twin studies have taught us much about the familial transmission of ADHD and its comorbid disorders. Both clinical and epidemiological studies have documented that children and adults with ADHD are at increased risk for antisocial disorders, autism spectrum di- sorders (ASDs), anxiety disorders, mood disorders and substance use disorders. Except for some anxiety disorders, each of these disorders clusters together with ADHD in families. In fact, twin studies of childhood disorders indicate that about half of the comorbidity among these disorders is due to genetic factors. There have been many twin studies of ADHD and ASDs. As a group, they show that these two disorders share genetic risk factors. The fact that ADHD shares gene- tic causes with other psychiatric disorders is extremely important for clinicians to understand. Such data argue against the idea that when two disorders co-occur, only the “primary” disorder should be treated with the other disorder viewed as a secondary phenomenon. Therefore, current practice suggests that all disorders be treated sequentially starting with the most serious condition. 7 MOLECULAR GENETICS In the 1990s, molecular genetic studies of ADHD were mostly limited to candi- date gene association studies. The candidate genes were chose based on theories of ADHD’s etiology, most of which were driven by the observation that effec- tive drugs for ADHD modulate dopaminergic and noradrenergic circuits in the brain. Association studies pick a genetic marker that is in or near the gene and Figure 1.2 Percentage of ADHD in siblings and parents based on adoption studies. Data from Sprich et al. 3 Siblings Biologic Adoptive Control Parents Biologic Adoptive Control