The central paradox of schizophrenia is that the condition, apparently genetic in origin, persists in spite of a substantial fecundity disadvantage. The hypothesis is proposed that the predisposition to schizophrenia is a component of Homo sapiens-specific variation associated with the capacity for language. A genetic change (the 'speciation event', predicted to be related to the Xq21.3 to Yp chromosomal transposition that separates Homo sapiens from the great apes) allowed the hemispheres to develop with a 'cerebral torque', reflected particularly in association cortex, from right frontal to left occipital. Variations in the dimension of lateralization are associated with differences in the rate at which verbal and non-verbal ability develops. The nuclear symptoms of schizophrenia can be understood as a failure to establish dominance for a key component - the phonological sequence - of language in one hemisphere, with consequent disruption of the mechanism of 'indexicality' that allows the speaker to distinguish his thoughts from the speech output that he generates and the speech input that he receives and decodes from others.