Mental Diseases Are Metabolic

Introduction
In 1920 psychoanalysis was in high fashion despite criticism from Emil Kraepelin of Germany. The German approach was largely to use neuropathology to study mental disease. In 1931 W. Spielmeyer addressed "The problem of the anatomy of schizophrenia" in a paper. Indeed it was a can of worms.
Kraepelin favored the medical model, which was supported by the brilliant work of the Italian scientist Buscaino in 1921. Buscaino reported grapelike formations in the brains of schizophrenics. Josephy (1930) reported cell sclerosis and fatty degeneration in the cortical layers.

Early Twentieth Century Medical Science
In the 1940's a brilliant American star was rising. His name was Linus Pauling.
The Vogts found anatomical variations in all cases of schizophrenia. They reported a progressive disintegration and disappearance of the tigroid substance and an increase in fat content (as well as other findings) in schizophrenia. Vacuolation of the cytoplasm was reported.

Neuropathology Reflects Metabolic Errors

The Vogt family, including Cecile & Oskar Vogt of Germany and Marthe Vogt of Edinburgh, Scotland, used neuropathology to try to ferret out the metabolic errors that cause disease. In 1951 C. Vogt & O. Vogt reported a study of Huntington's chorea and schizophrenia. Huntington's chorea is hereditary. They reported pathology in the striatum in schizophrenia. Most of the cells were damaged. They were wasting cells, or "schwundzellen". Their cytoplasm became progressively vacuolated and then disappeared whereas "their nucleus remained relatively unaltered".

Heath's Neurophysiological Approach

Heath used both biochemical methods and neurophysiological methods. He studied the septal area of the brain because he found abnormal electrical effects in this area in schizophrenics. The patients showed classical psychotic symptoms when the recording abnormalities appeared on the depth EEG. He implanted electrodes in the brain. Septal spiking was seen. This technique was used as an assay for a serologic fraction extracted from the blood of schizophrenics, which he named "taraxein". The fraction was injected into monkeys, which then showed severe behavioral symptoms. At first Heath thought the fraction was similar to ceruloplasmin, an alpha-2-globulin. Further study showed it to be a different globulin. This work was confirmed by Hoagland et al, who thought that there was a tightly bound small molecule attached to the globulin.

Lozovskii et al (1977)
This Russian group reported increased serum lactate dehydrogenase activity in schizophrenia. They reported that this effect was due to "additive polygenic inheritance with threshold manifestation". Twins were studied. Some of the twins were dizygotic and some of the twins were monozygotic (identical). There was a correlation between enzyme activity in schizophrenics and in their relatives. This correlation was "marked".
Mukhin & Faktor (1979)
This work continued the previous Russian work and may explain why the enzyme was high. Mukhin & Faktor reported a "stimulating effect of schizophrenic patients' plasma on the cellular incorporation of tryptophan". Hemolysis was seen perhaps due to flooding of the erythrocytes with tryptophan, which is an amino acid. Hemoglobin was released from the erythrocytes, suggesting that the cell membranes were ruptured. The cytoplasmic enzyme lactate dehydrogenase was increased. This suggests that the tryptophan was converted into alanine and then into pyruvate, which in turn can be converted into lactate. Thus at least one amino acid is flooding the glycolytic pathway.
Phenylketonuria
This disease is an inborn error of metabolism which results in mental retardation. In 1998 Shiwach & Sheikha reported "delusional disorder in a boy with phenylketonuria ..." "He did not respond to a traditional antipsychotic medication ..." The authors considered him "dually diagnosed". They felt that this case supported "the prevalent biogenic amine theories in psychiatric disorders". However, this author (Olson) feels that the case supports the amino acid flooding theory of schizophrenia. According to this theory, amino acids flood the brain cells in schizophrenia causing a disruption of carbohydrate metabolism. In other words, amino acids are burned for fuel by the brain instead of glucose with disastrous results. In this case the amino acid flooding the brain is phenylalanine.
Conclusions

The findings of the Vogts represent very important clues. The fat deposits are explained if amino acids are flooding the cells. The Vogts themselves were unable to figure this out. The destruction of the tigroid substance is also explained by this theory. The tigroid substance houses amino acids for the production of proteins.
It would appear that a diet very low in amino acids should be tried as a treatment.
Bibliography
1. http://www.associatedcontent.com/article/1232896/phytochemicals_to_fight_diseases.html
2. www.associatedcontent.com/article/1233607/postmortem_studies_of_the_schizophrenic.html
3. www.associatedcontent.com/article/1225494/microscopic_brain_lesions_in_schizophrenia.html
4. www.associatedcontent.com/article/1229893/neuropathological_findings_in_schizop