**7. Genetic explanations**

One of the most persuasive explanations is that a genetic predisposition may lead to abnor‐ mal neurological development, which in turn may manifest in various different aberrant be‐ haviors and developmental delays. As autism, ADHD and dyslexia and other developmental conditions are all highly heritable, so they all have a large genetic compo‐ nent, the theory seems plausible. The same genetic anomaly may lead to several disorders or psychiatric conditions. In other words one genotype may lead to several (related) pheno‐ types. This is known as 'pleiotropy'. Researchers have suggested that co-occurrence of au‐ tism and ADHD (and other developmental disorders) may reflect such common genetic causes (Reierson et al, 2008). In this model, the origins of both sets of difficulties are due to common genetic anomalies that predispose children to delayed or atypical neurological de‐ velopment. Certainly, specific genetic anomalies have been associated with a range of psy‐ chopathologies in adulthood. However, the genetic picture is complex and exact pathways are not established. It is estimated there are more than a thousand gene variations which could disrupt brain development enough to result in social delays (Sanders et al., 2012).

Such a genetic predisposition is almost certainly complex and multi factorial. So far, over 100 candidate genes have been associated with ASD, most of which encode proteins in‐ volved in neural development, but exact mutations within the candidate genes have yet to be identified (Freitag, 2007). Furthermore, different individuals may have mutations in dif‐ ferent sets of genes and most of the discovered gene variations are likely to have a low pene‐ trance, thus not all carriers will develop the disorder. There may be interactions among mutations in several genes, e.g. between regulatory genes and coding regions, or between the environment and mutated genes, altering their expression. The effect of a mutation or deletion can depend on processes relating to gene expression and regulation as well as the subsequent effects on the expression of other genes.

The advent of genomics and the emphasis placed on this has led to much research to identi‐ fy genetic predispositions to ASD. The field of psychiatry as a whole has been 'geneticised' according to some social theorists. This refers to the potential reclassification of psychiatric conditions in the light of findings from molecular biology. For example, a particular sub-cat‐ egory of DSM-IV schizophrenia has been linked to a substitution of a single base in the se‐ quence of DNA of a particular gene localised to a precise place on a particular chromosome, leading to a substitution of one amino-acid for another in an enzyme involved in neuro‐ transmission. Hedgecoe (2001) provides a discussion of the geneticisation of schizophrenia. The debate as to whether the old psychiatric systems of classification should be overhauled in the light of new genomic knowledge which illuminates genetic aetiologies is ongoing (Ericson & Doyle, 2003).
