The important role of environmental regulation of gene expression, i.e., part of the field of epigenetics, remains a challenge to the neurodevelopmental theories proposed by such theorists as Daniel Weinberger and others. Arturas Petronis (2004), in his “Schizophrenia, neurodevelopment, and epigenetics” in Neurodevelopment and Schizophrenia edited by M. Keshavan, J. Kenennedy & R. Murray and published by Cambridge University Press, note:

“There is one key issue that the epigenetic theory treats differently to the neurodevelopmental approach. From the epigenetic point of view, age- and hormone-dependent neurochemical changes [e.g., excessive cortisol expression associated with acute and chronic stress/anxiety] rather than structural changes in the brain are the main disease mechanism. Brain morphological aberrations are more likely to be just the reporters of mild deviation in the developmental program rather than factors causing or predisposing to schizophrenia. There is strong reason to believe that those early and minor developmental aberrations can be fully compensated by the developing brain, which exhibits surprising plasticity and compensatory potential (Kolbs, 1995; Woods, 1998). The shift from the brain structural peculiarities to the functional ones is consistent with the rare but very informative cases of monozygotic twins discordant for schizophrenia, where brain anomalies are more severe in the unaffected twin (Torrey et al 1999, Fig. 6.4 on p. 114). The subtle localized non-progressive prenatal brain developmental aberrations are just like superficial scars, which do not do any harm but only remind of an old minor injury. The problem of latency of the developmental changes-one of the main unclear issues in the neurodevelopmental theory-can now be formulated into the latency of epigenetic misregulation of some critical genes” (p. 187).

Brian Koehler PhD
New York University