Schizophrenia is a serious and devastating mental illness. Contrary to popular belief, the disease is characterized by paranoid delusions, hallucinations, or disordered thinking and behavior, rather than a “split personality.” While the symptoms can be reduced with medication, schizophrenia is a lifelong condition with no known cure.
Experts believe that a combination of genetic predisposition and environmental factors such as stress or childhood trauma can cause the disease to manifest later on in life. Gluten may also be a factor in schizophrenics with celiac disease.
Homocysteine levels are another environmental factor that can influence development of the illness, according to a new study conducted by Japanese researchers. Previous studies have cited high levels of plasma homocysteine (hyperhomocysteima) as a potential risk factor for schizophrenia. But since independent factors such as smoking and folate deficiency could have created false associations, a definite causal relationship hadn’t been established.
The authors analyzed over 30 published papers to look for a direct causal relationship. Specifically, they looked at papers describing the MTHFR C677T polymorphism, a mutation that results in reduced enzyme efficiency and higher plasma homocysteine levels. They used a special statistical technique based on participant genotypes to get a clearer picture of the data. Using this technique, the authors found that plasma homocysteine levels had a significant effect on schizophrenia risk.
Their findings align with related studies, such as one reporting that hyperhomocysteima in pregnant women during the third trimester increased the risk of schizophrenia in their children. Other papers have reported that reducing homocysteine levels with folate, vitamin B12, and pyridoxine treatment can reduce symptoms of schizophrenia.
While the research identified a link between the MTHFR C677T mutation and schizophrenia, the study has its limitations. For example, it’s possible that a single mutation could affect multiple (otherwise unrelated) traits, which could confuse the results. It’s also possible that the body compensates for the mutation during its development, so that it doesn’t end up being expressed at all. While the study used a mixed population, people of different ethnicities or ages may have different genetic or physiological predispositions. And several other mutations may also play a role in hyperhomocysteima. More research is needed to sort out all the variables, and confirm MTHFR’s role in the development of schizophrenia.
The paper, published in the journal BMC Medical Genetics, is available for free online.
