World J Psychiatry Ment Health Res | Volume 6, Issue 2 | Research Article | Open Access
Morris JA1*, Wray M2, Nicholls K3 and Rigby RJ3
1Education Centre, University Hospitals of Morecambe Bay NHS Trust, Royal Lancaster Infirmary, UK 2Kirkstone House, Murley Moss Business Park, UK 3Department of Health & Medicine, Lancaster University, UK
Fulltext PDFSchizophrenia is a condition in which biopsychosocial factors interact with genetic pre-disposition to cause a disease of thought disorder. It is proposed that bacterial induced inflammation and toxemia, a consequence of mucosal tissue dysbiosis, is one of the key environmental factors in the pathogenesis of schizophrenia. Genetic polymorphisms identified in schizophrenia include genes involved in immunity. The age incidence and sex ratio seen in schizophrenia are consistent with previously published models of bacterial infection. Mucosal tissue dysbiosis induced inflammation can explain the key associated features of neuroinflammation, periodontitis, low levels of vitamin D, accelerated aging, and early life developmental changes. Mucosal tissue dysbiosis induced inflammation is orchestrated by cytokines as are emotional responses. This gives a plausible mechanism for biopsychosocial interaction in the genesis of thought disorder. Mucosal tissue dysbiosis induced inflammation can be investigated by using PCR (polymerase chain reaction) to assess the carriage of specific bacterial pathogens in cases and controls. Optimizing the microbial flora from early in life could reduce the severity of the disease. This could be achieved by simple measures, such as maintaining serum vitamin D levels and regular consumption of yoghurt.
Schizophrenia; Mucosal tissue dysbiosis; Neuroinflammation; Periodontitis; Vitamin D; Yoghurt
Morris JA, Wray M, Nicholls K, Rigby RJ. Mucosal Tissue Dysbiosis Induced Inflammation Interacts with Psychosocial Factors and Genetic Factors to Cause Schizophrenia. World J Psychiatry Ment Health Res. 2023;6(2):1036..