Table of Contents
ISRN Psychiatry
Volume 2013, Article ID 604587, 10 pages
Research Article

A Novel Model of Schizophrenia Age-of-Onset Data Challenges the Conventional Interpretations of the Discordance in Monozygote Twin Studies

1Physics Department, University of Maryland Baltimore County, 1000 Hilltop Circle, Catonsville, MD 21250, USA
2Maryland Psychiatric Research Center, University of Maryland School of Medicine, P.O. Box 21247, Baltimore, MD 21228, USA

Received 21 May 2013; Accepted 7 July 2013

Academic Editors: S. Chakrabarti and S. Lawn

Copyright © 2013 Ivan Kramer and L. Elliot Hong. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The relative importance of genetics and the environment in causing schizophrenia is still being debated. Although the high proportion of monozygote cotwins of schizophrenia patients who are discordant suggests that there may be a significant environmental contribution to the development of schizophrenia, this discordance is predicted by an accumulative multimutation model of schizophrenia onset constructed here implying a genetic origin of schizophrenia. In this model, schizophrenics are viewed as having been born with the genetic susceptibility to develop schizophrenia. As susceptible gene carriers age, they randomly accumulate the necessary mutations to cause schizophrenia, the last needed mutation coinciding with disease onset. The mutation model predicts that the concordance rate in monozygote twin studies will monotonically increase with age, theoretically approaching 100% given sufficient longevity. In dizygote cotwins of schizophrenia patients, the model predicts that at least 71% of cotwins are incapable of developing schizophrenia even though every cotwin and their schizophrenic twin shared a similar early environment. The multimutation model is shown to fit all of the monozygote and dizygote concordance rate data of the principle classical twin studies completed before 1970 considered in this paper. Thus, the genetic hypothesis of schizophrenia can be tested by bringing these studies up to date.