Psychosis can be conceived as a continuum extending from unipolar through bipolar affective and schizo-affective disorder to schizophrenia with varying seventies of defect. The continuum has a degree of stability in that relatives of probands at a particular point on the continuum are at risk of illnesses of a similar type, but there is also the possibility of change. Some evidence suggests change takes place between generations, perhaps particularly in the direction of increased severity. The hypothesis is proposed that psychosis results from aberrations of the genetic programme for the development of cerebral asymmetries, these asymmetries being a particular feature of human evolution contributing to the capacity for communication and social interaction. The development of cerebral asymmetries is postulated to depend upon a specific interaction between a genetic sequence which has potential autonomy (e.g. a retrovirus or other mobile genetic element) and a growth factor, or proto-oncogene. The interaction and its high variability is preserved by evolutionary pressures; the persistence of the psychoses (and their variation in form) is viewed as an unfortunate by-product of this ‘hot-spot’ of genetic change.