Schizophrenia is a mental disorder characterized by an interruption of thought processes and by a deficit of appropriate emotional responses.
Common complex symptoms of the disorder include auditory hallucinations, paranoid delusions, and disorganized thinking. The onset of symptoms typically occurs in young adulthood and can significantly contribute to social and occupational dysfunction. However, the symptoms of the disorder can appear in infancy and childhood.
Social problems such as long-term unemployment, poverty, and homelessness as well as substance abuse are common. The average life expectancy of people with the disorder is 12 to 15 years less than those without, typically due to a higher suicide rate.
Schizophrenia is often confused with split personality or multiple personality disorders (dissociative identity disorder). The condition is more of a splitting of mental functions because of the symptomatic presentation of the illness. It effects cognition and contributes to chromic behavior and emotional problems. People suffering with schizophrenia are likely to have a comorbidity of depression or anxiety disorders.
Genetics, early developmental environment, and psychological and social processes contribute to the onset and persistence of the condition. Recreational and prescription drug use can improve or worsen symptoms. Recent research has been focused on the role of neurobiology, though no single primary organic cause has been isolated. Stress can exacerbate the disorder.
Treatment for schizophrenia requires the application of prescribed antipsychotic medication. These psychotropics primarily suppress dopamine and serotonin receptor activity. Psychotherapy is also an important component of treatment. Sufferers are more of a risk to themselves than they are to others but can demonstrate and lash out with erratic violent outbursts. Often involuntary hospitalization may be necessary in order to rehabilitate a schizophrenic, regulating medication.
According to new research, disclosed in an issue of the Journal of the American Medical Association (JAMA) of Psychiatry, adding the dietary supplements folate and vitamin B12 to antipsychotics may improve symptoms. Often medication alone is ineffective in debilitating cases.
The study, performed by a team based at Massachusetts General Hospital (MGH), focused on the negative symptoms of schizophrenia which include apathy, social withdrawal, and a lack of emotional expressiveness.
Folate (folic acid) is an essential nutrient and is required for the synthesis of DNA and neurotransmitters, playing an important role in the control of gene expression. B12 has been found to metabolically amplify the effects of folic acid.
Adequate folate intake during pregnancy can reduce the risk of birth defects. Studies have suggested a deficiency in folate during pregnancy significantly increases the risk of schizophrenia among offspring. Earlier research by members of the MGH-based team associated low-blood folate levels with more severe negative symptoms among patients with schizophrenia.
Current research was designed specifically to investigate whether supplementation with folate and B12 reduced negative symptoms of schizophrenia. In order to achieve a clear picture of folate’s effects on negative symptoms, researchers enrolled 140 schizophrenic patients at community mental health centers in Boston and Rochester, New York, and Grand Rapids, Michigan.
All participants involved in the study continued taking their respective antipsychotic medications and were additionally provided daily doses of either folate and B12 or placebos for 16 weeks. A placebo is a medically ineffectual treatment for a disease or condition intended to deceive the recipient. Sometimes patients given a placebo treatment will have a perceived or actual improvement in a medical condition, a phenomenon commonly called the placebo effect.
Every two weeks during the 16 week trial, patients were evaluated using standard assessment tools. Blood levels were measured for folate and homocysteine (associated amino acid). Outliers in individual dietary nutritional information were accounted for.
It was determined while the level of improvement across all participants was modest, enhanced symptomatic tempering was more significant in individuals carrying specific variants in genes associated with folate metabolism in those receiving folate and B12.
Dr. Joshua Roffman of the MGH Department of Psychiatry and corresponding author of the JAMA Psychiatry paper, revealed:
“Our finding that folate plus vitamin B12 supplementation can improve negative symptoms opens a new potential avenue for treatment of schizophrenia. Because treatment effects differed based on which genetic variants were present in each participant, the results also support a personalized medical approach to treating schizophrenia.”
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