Schizophrenia Daily News Blog

Schizophrenia probability model

Does god play dice with schizophrenia? A probabilistic model for the understanding of causation in mental illness
Marco Procopio, Medical Hypotheses (2005) 64, 872–877

It has been observed since the first descriptions of schizophrenia that there is a tendency for the illness to run in families. An observation like that gives credence to a genetic theory of inheritance. However, it has also been observed that even in people with identical genes (Identical twins) there is only a 50% concordance (meaning 50% of the time that one identical twin has schizophrenia the other twin does as well.) If schizophrenia were purely genetic, there would be a concordance approaching 100%. Therefore there must be some nongenetic component to the development of schizophrenia. Researchers and theorists have debated what this contribution is. This article poses a new idea for the genetic model.

We’ve talked about many of the possible theories on these pages before. A leading theory is called the “second-hit” theory. This means that there is a “first hit” from a genetic component that predisposes a person to developing schizophrenia. There must then be a “second hit” – perhaps an obstetrical complication/infection, drug use, social stressor, etc that leads to the development of the schizophrenia syndrome.

The author of this study is proposing a probability based model for the development of schizophrenia. He points out that schizophrenia is a neurodevelopmental disease that likely originates in utero therefore ruling out the possibility that environmental factors could contribute short of having something that affects the mother during pregnancy. Rather than considering it the role of the environment that explains the reason that identical twins only have a 50% chance of concordance, he likens the model to that of nuclear decay. In nuclear decay, molecules that are identical have a random chance of undergoing decay. In essence, there is just a certain amount of randomness in the system. He also explains that there are many genes responsible in some part for schizophrenia and that as one accumulates the more schizophrenia-prone copies, the risk increases exponentially rather than linearly. In this manner, those with the most genes at risk for schizophrenia are at a substantially higher risk but that there is still some randomness that allows for full development of the syndrome.

This article is interesting in that it presents a different perspective on risk of schizophrenia and the role that genetics and the environment play in the development of the disease. While it is not a prevailing theory, it is interesting nonetheless.

Click here to access the article on PubMed