The idea that gluten consumption may influence the development of schizophrenia has been the subject of a bit of discussion lately (1). Much of the speculation comes from the increased rates of gluten intolerance and celiac disease like symptoms found in schizophrenics (2,3). One major hypothesis postulates that when gluten derived peptides known as exorphins enter the blood they disturb brain function and cause schizophrenia (4,5). And while there is a correlation between gluten intolerance and schizophrenia, it’s merely that; a correlation. Not much evidence exists proving causality. It is possible that gluten is responsible, but it could be that both are symptoms of the same underlying cause. Let me explain.
There is increasing evidence that schizophrenia has an important connection to arachidonic acid. It’s often noticed that schizophrenic people are less susceptible to arthritis, the flushing effect of niacin, and pain. All these processes involve the release of AA from cell membranes and subsequent conversion of AA to proastaglandins. Finally, fevers have been known to improve symptoms of schizophrenia. Fevers promote the release of arachidonic acid from cell membranes. David Horrobin presented this, along with other observations, as evidence that prostaglandin deficiency may be playing a casual role in the development of schizophrenia (6,7,8).
So what is connection to gluten? Well, Chris Masterjohn wrote in his article Good Fats, Bad Fats that “Inhibiting supposedly “inflammatory” products made from arachidonic acid such as prostaglandin E2 using over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs) can produce a number of inflammatory outcomes. These drugs induce intestinal pathologies that closely resemble celiac disease in laboratory animals in response to gluten or even egg white” (9).
So given that, perhaps one of the same underlying contributers to schizophrenia is also contributing to the increased rates of gluten intolerance seen in people with schizophrenia, namely prostaglandin deficiency.
However, it’s also possible both theories even reinforce each other. It could be and that prostaglandin deficiency causes intestinal permeability and allows neuroactive peptides to move from the gut to the blood stream and finally to the brain. I’m speculating like crazy right now, so I’m gonna have to get into the scientific literature for a while and come back to this. More in my next post.