The Microscopy of Schizophrenia

In 1986 Kleshchinov & Oifa reported a postmortem study on schizophrenics. They found "cytoplasm lightening" and gradual lightening of the nuclei. There was swelling of the cysterns of the endoplasmic reticulum and loss of polysomes. My own interpretation of these results is that amino acids are housed in the cysterns, so a flooding of the cysterns with amino acids would explain everything. There would be a drain of RNA from the nucleus, which would explain the lightening of the nuceus. The polysomes might be consumed by excessive production of protein (to try to get rid of some of the excess amino acids).

Uranova (1988)

Uranova reported "pathologic changes". She found "pronounced swelling" of the dendrites. She found "mitochondria swollen". These findings were in the "prefrontal cortex". These findings are also consistent with amino acids flooding the cells. The mitochondria take up amino acids.

Hirata-Hibi & Hayashi (1993)

These Japanese workers found "the P lymphocyte", which is "a stimulated atypical lymphocyte that is found in schizophrenics". The cytoplasm often contains vacuoles. Since vacuoles are usually food or fat, this is consistent with the amino acid theory. Some amino acids could be converted to fat.

Oifa & Uranova (1991)

These Russian workers found "foci of neuronal loss" and "swollen dendrites".

Stress

Oifa & Kleshchnov (1985) stressed rats and reported "acute neuronal swelling". There was "complete dissociation of polysomes, swelling of some cisterns of the endoplasmic reticulum and perinuclear space, and destruction of the mitochondria".

Mazzarello et al (2004)

These Italian workers found "a cytoplasm rich in free ribosomes and polysomes" in the lymphocytes of schizophrenics.

Kokai et al (1998)

These Japanese workers also reported atypical lymphocytes in schizophrenia. They found "blast-type atypical lymphocytes" in schizophrenia. These were "stimulated or activated cells". These cells were large.

Orlovskaia et al (1975)

These workers reported "damages of membranes, mitochondrias, and accumulation of granular material in the cytoplasm". This could be explained by a toxic factor that attacks the cell memranes. Such a factor might have some fat solubility because the membranes are made of fat. The granular material could be glycogen.

Mitochondrial Dysfunction in Schizophrenia

Several reports have appeared in the professional literature implicating mitochondrial dysfunction as causing schizophrenia. In March 2001 a report appeared in Schizophrenia Research by Maurer et al of Germany. This paper reported "evidence for a mitochondrial oxidative defect in brains of patients with schizophrenia".

Maurer et al (2001)

This report claims "an impairment of energy metabolism in brains of patients with schizophrenia". "Decreased oxidative metabolism has been consistently documented in the frontal lobes." Measurements by the German group "confirm a defect of oxidative phosphorylation in brains from patients with schizophrenia, which may contribute to impaired energy generation". Post-mortem brain specimens were used. The maximum reductions were in the frontal cortex, the temporal cortex, and the basal ganglia. There was no reduction in the cerebellum.

Ben-Shachar (2002)

This report came from Israel. Ben-Shachar recommended ""novel treatment approaches". The author suspected "linkage to dopamine". The author claimed "altered cerebral energy metabolism".

Uranova and Aganova (1989)

This report related the results of microscopic analysis of autopsy specimens. They reported deformation and reduction in the number of mitochondria. Similar results were reported by Kung and Roberts (1999). Kolomeet and Uranova (1999) reported similar findings.

Prabakaran et al (2004)

This report appeared in Molecular Psychiatry. The University of Cambridge group in England reported "mitochondrial dysfunction in schizophrenia". They used techniques called transcriptomics, proteomics, and metabolomics. They reported "confounding drug effects could be ruled out".

"Altered proteins" were reported by the British group. They suggested "compromised brain metabolism". This is certainly food for thought. What to do in the way of treament is not yet clear, unfortunately.

Advances in Neuropsychiatry

There are a number ot textbooks on neuropsychiatry, including Yudofsky & Hales. The fourth edition of this brilliant book came out in 2002. Although the editors are Yudofsky & Hales, many different authors are used in the various chapters of this comprehensive text. The down side of the book is that there is no mention of orthomolecular treatment.

Tamminga et al (1992)

This brilliant group did PET studies of brain glucose metabolism. Young, drug-free, "floridly psychotic individuals" were studied. They found reduced metabolism in limbic structures in schizophrenia. This appears to strongly support the work of Heath of New Orleans, who reported depth EEG abnormalities in limbic structures. These abnormalities were caused by an unknown toxic factor in the blood which he called "taraxein".

Panic Disorder

Liebowitz etal (1985) reported that lactate infusions caused panic attacks in patients with panic disorder. This brilliant study may be very important because it could mean that there is an error in lactate metabolism in these patients. In other words, the patients may have already high lactate in their brains. The additional lactate from the infusion sets off the panic attack.

Psychiatry

In 2003 the two volume set called "Psychiatry" was edited by Tasman, Kay, and Lieberman. This book, like the Yudofsky & Hales book, has chapters by many authors. It traces psychiatry back to the days of Esquirol (1838). Esquirol was a French psychiatrist and author.

Conclusions

It appears that an unknown toxic factor in the blood causes a flooding of the cells with amino acids. This factor may be a stress chemical. A low protein diet is suggested.

Drugs have been used. Unfortunately some drugs can cause birth defects. Other harmful side effects are also seen. Hippocrates wrote, "Do no harm."

Also it is probably a good idea to avoid stress. Stress may play a role in the etiology of schizophrenia.

Many of my references came from the website Pubmed. For further information, either consult Pubmed or the following bibliography:

Bibliography

1. www.associatedcontent.com/article/723727/an_endogenous_inhibitor_of_monoamine.html
2. www.associatedcontent.com/article/722243/schizophrenia_an_error_in_homeostasis.html
3. www.associatedcontent.com/article/721845/phytochemicals_for_schizophrenia_cancer.html

4. www.associatedcontent.com/article/717973/progressive_brain_tissue_loss_in_schizophrenia.html