There may be a schizophrenia-specific, genetically enhanced affinity for exorphins by opioid receptors influencing dopaminergic and other neurons.
Genetic hypothesis of idiopathic schizophrenia: its exorphin connection.
AI Summary
Key Findings
Abstract
This brief overview proposes a testable oligogenic model of the inheritance of susceptibility to idiopathic schizophrenia:"abnormal"genes at each of a few complementary loci. The model is based on my assumptions as to the likely genetic abnormalities at possibly four or five interacting loci that would permit exorphins, the opioid peptides from some food proteins, especially glutens and possibly caseins, to go from gut to brain and cause symptoms of schizophrenia. Exorphins may reach the brain cerebrospinal fluid (CSF) in harmful amounts because of their genetically increased, receptor-mediated transcellular passage across the gut epithelial barrier plus decreased catabolism by genetically defective enzymes. A schizophrenia-specific, genetically enhanced affinity for exorphins by opioid receptors influencing dopaminergic and other neurons would permit sustained dysfunction at low CSF exorphin concentrations. Tests of each postulated genetic abnormality are suggested. This model is supported by a variety of evidence, including a significant effect of gluten or its absence on relapsed schizophrenic patients, the high correlation of changes in first admission rates for schizophrenia with changes in grain consumption rates, and the rarity of cases of schizophrenia where grains and milk are rare.
Affiliation
Medical College of Pennsylvania, Eastern Pennsylvania, Psychiatric Institute, Philadelphia 19129.
External References
- PubMed ID:
- 2851166
Comments
Sign in or create a free account to join the conversation.
Sign in to commentBe the first to comment.