## 2 Why the Electroencephalogram (EEG)?
### qEEG Heritability  
A large body of studies have suggested that qEEG characteristics and their variability are largely determined by genetics and, thus, are highly heritable (up to 90%) [79; 80; 81; 82; 83; 84; 85; 86; 87; 88; 89; 90; 91; 92; 93]. Additionally, it was demonstrated that the correlations for qEEG characteristics between family groups (each consisting of a biologically related father, mother, and two children) were greater than those obtained from the non-family groups (each consisting of biologically unrelated subjects) [94] (see also [89]). Smit et al. [92] proposed several common genetic sources for EEG: (a) skull and scalp thickness may affect the conductive properties of the tissues surrounding the cortex, (b) genetic influence on cerebral rhythm generators such as the central 'pacemaker' in the septum for hippocampal activity or the thalamocortical and corticocortical generators of cortical rhythmicity, (c) genes directly involved in the bioelectric basis of the EEG signal itself: for example, genes influencing the number of pyramidal cells, the number of dendritic connections, or their orientation with respect to the scalp may directly influence the mass dendritic tree depolarization of pyramidal cells in the cortex that underlies the EEG. Begleiter and Porjesz [95] added another factor: regulatory genes that control the neurochemical processes of the brain and, therefore, influence neural function. Besides high qEEG heritability, genetic loci underlying the functional organization of human neuroelectric activity and their associated conditions/behavior have also been identified. Below is a short overview of qEEG oscillations, the related genes, and the associated pathological conditions:  
1. qEEG beta oscillations (_beta rhythm_ is electromagnetic oscillations in the frequency range of brain activity above 13 Hz)
2. Winterer et al. [96] reported that three exonic variants of the gene encoding the human gamma-amino butyric acid (GABA)\({}_{\text{B}}\) receptor on chromosome 6 modify the cortical synchronization measured as scalp-recorded qEEG coherence. Another genetic study indicated the importance of GABA\({}_{\text{A}}\) receptor genes in the modulation of qEEG beta oscillations in the human brain: Porjesz et al. [97] found a significant genetic linkage between the beta frequency of the human qEEG and a cluster of GABA\({}_{\text{A}}\) receptor genes on chromosome 4p. Additionally, this same GABA\({}_{\text{A}}\) receptor gene was found to be associated with a DSM-IV diagnosis of alcohol dependence [98]. 3. qEEG alpha oscillations (_alpha rhythm_ is electromagnetic oscillations in the frequency range of 8-13 Hz, arising from the synchronous and coherent electrical activity of neurons in the human brain)  
Low voltage qEEG alpha oscillations have also been reported to be linked to (a) the GABAergic system, as an association has been found between the exon 7 variant of the GABA\({}_{\text{B}}\) receptor gene and alpha voltage [99], (b) a serotonin receptor gene (HTR3B), associated with alcoholism and antisocial behavior [100], and (c) a corticotrophin-releasing binding hormone (CRH-BP) [101; 102], associated with depression, anxiety, and alcoholism. Low voltage alpha in females has also been reported to be associated with a genetic variant that leads to low activity of the enzyme that metabolizes dopamine and norepinephrine, catechol-o-methyltransferaseanferase (COMT) [103]. Additionally, low voltage alpha has been associated with a subtype of alcohol dependence with anxiety disorders [104; 105] and with the brain-derived neurotrophic factor (BDNF) Val66 Met polymorphism in depression [106]. High voltage qEEG alpha oscillations are heritable in a simple autosomal dominance manner [79]. The alpha peak frequency (APF) has been associated with the COMT gene, with the Val/Val genotype being marked by a 1.4 Hz slower APF compared to the Met/Met group [107].