Schzophrenia

The content of this article is from the book “The Comprehensive Guide to Glutathione”
by Dr. Jimmy Gutman MD FACEP

The Greek meaning of schizophrenia “split mind” is misleading. The disorder should

not be confused with split personality multiple personality disorder. It is a different

illness characterized by psychosis-a severe disturbance of normal thought, perception,

speech and behavior. In mood disorders like anxiety and depression, the ability to discern

the real from the imagined is relatively intact. A schizophrenic patient on the other hand

often suffers from delusions, auditory visual hallucinations, and paranoid thoughts

not based on reality. Although there is no consensus as to the causes of schizophrenia, most specialists

agree that its symptoms stem from a disturbance of normal brain chemistry. Schizophrenia seems to run in families, and yet no single schizophrenia gene has been identified. Psychotherapy alone is not enough.

Antipsychotic drugs have been able to reduce relapses by 50%, and to considerably shorter

the periods of hospitalization. However, these drugs have significant side effects and long-term complications. It has long been known that glutathione levels are lower in schizophrenic patients.

Researchers have consistently demonstrated increased oxidative stress and decreased

glutathione status in their brains. Glutathione levels fall as the disease grows more severe.

The Russians NV and AV Govorin showed that during an acute phase of their disease,

schizophrenics suffer higher levels of lipid peroxidation than when they’re in remission.

Research scientists such as Yao and Reddy of the Veteran’s Administration Healthcare

System, University of Pittsburgh suggest that oxidative stress plays an important

pathophysiological role in schizophrenia.

A group of neurochemicals called catecholamines are normally produced by the body,

but over-produced in schizophrenia as well as Parkinson’s disease. The catecholamines

break down into ortho-quinones—a group of powerful oxidants. Baez’s team at the

Department of Biochemical Toxicology in Stockholm University examined glutathione’s ability to detoxify these metabolites. They concluded that glutathione enzymes provided critical protection against the neurodegenerative diseases that are caused or conditioned by these dangerous oxyradicals.

Buckman and Kling at UCLA School Of Medicine conducted a fascinating study in which CT-scans of schizophrenic patients revealed brain atrophy (shrinkage), suggesting damage to nerve tissue. They correlated the extent of atrophy to the degree of glutathione peroxidase deficiency. This suggests a unique function of glutathione in

preserving the brain from tissue damage in schizophrenics. These findings were corroborated at other centers, such as Hahnemann University in Philadelphia.

 More recently, researchers have demonstrated that determining a patient’s glutathione status could be helpful for diagnosing schizophrenia. Since it’s already established that abnormality low glutathione levels go along with schizophrenia, a multinational team (from Australia, Austria, Germany and Korea) measured glutathione levels to

determine patients’ long-term prognosis. After following their group of patients for seven years, they were able to successfully predict the development of their psychosis.

Taking advantage of recent developments in brain scanning a Japanese team used Magnetic Resonance Spectroscopy (MRS)’ to measure glutathione brain levels in living patients. As expected, lower glutathione levels correlated with the severity of the schizophrenic symptoms.

Until about 2008 the question remained, “Will raising glutathione levels in humans improve the condition of schizophrenia?” The researcher at the cutting edge of this strategy was Australian doctor Michael Berk who initiated a series of studies using the glutathione precursor NAC (N-acetylcysteine). Initially, he combined this intervention with standard schizophrenic antipsychotic medications. His success was evident in the results, and subsequent studies have added to the validity of his approach. A good review of NAC and schizophrenia can be found in the Annals of Clinical Psychiatry (Chen et al 2016).

Antipsychotic drugs require long term use and cause a number of side-effects. Haldol, Thorazine and other neuroleptics cause a movement disorder called tardive dyskinesia. This result in involuntary puckering of the lips and a writhing of the arms and legs that disfigures a large number of patients. It’s possible that lipid peroxidation accounts for neuronal damage in this disorder. Scientists have put this theory to the test.

A Scottish team led by Brown and Reid measured oxidative breakdown products and antioxidant depletion in diskenetic patients. They confirmed the relationship between lipid peroxidation and tardive diskinesia. Other researchers have shown that lipid peroxidation and glutathione depletion are aggravated by antipsychotic drugs. Sagara at the Salk

Institute in La Jolla, California said that eatmeinslular glutathione would aggravate haloperidol (a neuroleptic antipsychotic) toxicity, and may increase any tendency to tardive dyskinesia.

Researchers Cadet and Kahler from the National Institute of Health in Baltimore, as well as Mahadik and Scheffer from the Department of Health Behavior, Medical College of Georgia and others, have suggested that antioxidants should be used to prevent side effects in patients taking antipsychotics. The Georgia team also showed that oxidative injury increases and glutathione -peroxidase levels fall even at the earliest stages of psychosis, and that antioxidants may prevent or slow deterioration.

It appears that sustained glutathione levels may slow the progress of schizophrenia, improve symptomatology’ and decrease side effects of some of the drugs used against this disease.

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