Attention-Deficit/Hyperactivity Disorder and prenatal smoke and alcohol exposure

Abstract

Attention-deficit/hyperactivity disorder (ADHD) is a psychiatric disorder with an early life onset, which is clinically heterogeneous, and consists of several behavioural components. Structural brain imaging studies have shown that people diagnosed with ADHD have a smaller overall brain volume, and a wide variety of specific brain regions have been shown to be different from controls. Twin studies have found a relatively high heritability factor with an average of about 77%, thus 33% of the development of ADHD is accounted for by other factors, for instance in the environment. Environmental factors mostly associated with ADHD are adverse circumstances early in life, prenatally and shortly after birth. In this thesis earlier literature and results of an exploratory structural MRI study about the influence of prenatal alcohol and nicotine exposure on ADHD is reviewed. Special attention is paid to associated alterations in brain structure and gene/environment interaction. For prenatal smoke exposure there is strong evidence that specific genes related to the dopamine system amplify its effect on the risk of developing ADHD. This suggests that nicotine has its effects on development via modulation of the dopamine system, and thus increases the risk of ADHD when there is genetic predisposition. In contrast, only limited evidence is currently available for the possible role of prenatal alcohol exposure on the development of ADHD and is not sufficient to draw the conclusion that it does or does not increase the risk for ADHD.