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2 Rohde, Buitelaar, Gerlach & Faraone component. They also alert clinicians treating ADHD children that many of the parents of those children will also have ADHD, which could make it difficult for them to carry out instructions about how to implement medical or psychosocial treatments for their children. Because disorders can cluster in families due to environmental causes such as infections or mutual proximity to toxins, it is essential to consider adoption and twin studies when evaluating the possible genetic component to ADHD’s etiolo- gy. An example is shown in Figure 1.2. It shows that rates of ADHD are greater among biological relatives of non-adopted ADHD children than the adoptive re- latives of adopted ADHD children. The risk to adoptive relatives for ADHD was similar to the risk to relatives of children who did not have ADHD. 2,3 This finding suggests that it is the genetic relationship that mediates the familial transmission of ADHD. A more powerful method of separating genetic and environmental causes is the twin Study. Twin studies rely on a natural experiment. Identical or monozygo- tic (MZ) twins share nearly their entire DNA. In contrast, fraternal or dizygotic (DZ) twins share, on average, 50% of their DNA. They are not more genetically similar to one another than ordinary siblings. By studying MZ and DZ twins, one can compute the heritability statistic, which quantifies the fraction of ADHD’s etiology that can be attributed to DNA variation. Here and elsewhere we use the term “DNA variation” rather than “genes” because much of our DNA does not consist of genes. Instead, it provides instructions that create special molecules that regulate how genes are expressed. There have been 37 twin studies of ADHD. For a review, see Faraone and Lar- sson. 4 When considered together, the twins studies of ADHD lead to a heritability estimate of 74%. This heritability of ADHD does not differ by sex and is the same for inattentive and hyperactive-impulsive symptoms. Twin studies have also been able to test if ADHD is best described as a categorical disorder or a continuous trait in the population. This work suggests that ADHD is best described as a quan- titative trait that ranges from nonexistent and mild to moderate and severe. Under this model, the diagnosis of ADHD is the extreme of a trait that occurs in all indi- viduals. As we will discuss later, such data have clinical implications for how one should subthreshold cases of ADHD that are referred to clinical settings. Twin studies have also been used to shed light on the development and per- sistence of ADHD from childhood into adulthood. The heritability of clinically diagnosed ADHD in adults is 72%, which is similar to what is found in children. 5 As discussed in by Faraone and Larsson, 4 the heritability of ADHD is stable during the transition from childhood into adulthood, but both stable and dynamic genetic causes affect the expression of ADHD from youth to early adulthood. The stable component is a set of genetic risk factors that influence the expression of ADHD throughout the lifespan. The dynamic causes are genetic effects that turn on and off during development. These dynamic effects likely account for the variable age