Fetal Development and Schizophrenia: Historical Observations from Teratology

Abstract

A great deal of current interest about schizophrenia is centered upon the fetal development hypothesis: the suggestion that some challenge to a mother produces an error in development of her fetus which eventually results in schizophrenia in the child, now grown into a young adult. This hypothesis implicitly assumes several points. (1) Because the symptoms of schizophrenia are behavioral, we assume that the organ of the fetus which is finally affected must be the brain. We should remember that the initial challenge may act on the brain only indirectly, with a primary effect at some other tissue of either the mother or fetus. (2) Modern theories of embryonic development would suggest that the challenge to the mother would change the body chemistry of the mother and/or the fetus, thereby changing the makeup of the chemical milieu in which the fetus develops. Changes could involve the presence of chemicals which were not normally present, or the absence of — or perhaps simply alterations in the concentrations of — chemicals expected to be present. Certain of the chemical alterations must modify the structure of the fetus, probably by affecting the action of chemical inducers which regulate migration and/or differentiation of cells and cell accumulations.