An Endogenous Inhibitor of Monoamine Oxidase in Schizophrenia

Reports appeared in 1978 and 1980 by Philadelphia group claiming "an endogenous inhibitor of platelet MAO in chronic schizophrenia". The first report appeared in American Journal of Psychiatry. Berrettini and Vogel confirmed their work in 1980. They studied "platelet-free plasma obtained from chronic schizophrenia patients", which contained the inhibitor.

MAO

It seems that there are two types of MAO. Type B metabolizes phenyethylamine. Flavin appears to be a critical ingredient of MAO. Flavin comes from the vitamin riboflavin. Iron is also in the enzyme.
Neuropathology

Neuropathology studies indicate that something is abnormal. Figuring out what this abnormality is can be difficult. In 1897 Alzheimer described pallor and loss of pyramidal cells in the cortex of patients with "dementia praecox". In 1915 Southard reported atrophy in the cortical association centers. In 1948 and 1953 the Vogts reported cell gaps and other findings. Temporal horn enlargement has been repeatedly reported. This suggests tissue loss in the surrounding limbic structures, according to Bogerts et al (1985). Degreef et al (1992) reported increased incidence of cavum septi pellucidi. This finding appears to confirm Heath's location of schizophrenia in the septal area.

Amino Acids Flood the Brain in Schizophrenia

There is a chemical abnormality, but it is not completely clear what this abnormality is. The finding of gliosis by a number of investigators suggests an unknown toxic factor. The location of gliosis in subcortical areas of the brain high in dopamine suggests that the toxin could be a metabolite of dopamine. Such a toxin could use up MAO.

In 2001 Maurer et al reported "evidence for a mitochondrial oxidative phophorylation defect in brains from patients with schizophrenia". Other workers have documented decreased metabolism of glucose in the frontal lobes. Much of the energy generation takes place in the mitochondria. The Maurer study was done in Germany. They "analyzed spectrophotometrically postmortem brain specimens". They suggested "impaired energy generation". But what causes this to happen?

The Olson Theory

According to my theory, this problem is caused by a flooding of the brain cells with amino acids. Why is this important? It is of the utmost importance because it points towards a possible cure, which might be a diet very low in amino acids. The amino acids are being burned for fuel instead of glucose.

Depression

Centuries ago the term "melancholia" was used for what is now called "depression".

Kraepelin

Kraepelin was born in 1855 and died in 1926. Kraepelin may have been the first really great psychiatrist. In 1878 Emil Kraepelin was in Munich. At the same time Charcot was studying hysteria at the Salpetriere in France.

German Psychiatry

Whereas Wundt considered himself a psychologist, Kraepelin was a psychiatrist. Meynert was in Austria. Flechsig was a psychiatrist in Leipzig. Kraepelin published a number of books on psychiatry. Prior to Kraepelin, Pinel of France had been the most famous psychiatrist. Kraepelin defined "paraphrenia", a term previously used by Kahlbaum. He also used the term "dementia praecox". Neither term is used any more. Eugen Bleuler of Switzerland invented the term "schizophrenia", which is now popular.

Russian Psychiatry

Korsakov was born in 1854 and died in 1900. Another Russian psychiatrist of that era was Serbski. Swiss Psychiatry

For a small country Switzerland made great contributions to psychiatry. Eugen Bleuler was born in 1857 and died in 1939. Austria made many contributions, but many of them were bogus. Freud, Rank, Abraham, and Jones were from Austria.

American Psychiatry

Adolph Meyer came to the United States from Europe.

Alzheimer's Disease

In 1906 the German neuropathologist and psychiatrist Alzheimer described the disease which now bears his name. Plaques were found in the brain.

Putting the Pieces of the Puzzle Together

In 1897 the German scientist Kramer reported that the Nissl bodies were abnormal in "dementia praecox". This is an important piece of the puzzle. Since that time it has been found that the Nissl bodies take amino acids and convert them to proteins. The destruction of the Nissl bodies suggests an error in amino acid metabolism in schizophrenia, the new term for "dementia praecox". If the Nissl bodies were flooded with too many amino acids, this could cause destruction of the Nissl bodies.

But What Is the Cure, if Any?

It would seem that if amino acids flooding the brain cells causes schizophrenia, the logical treament would be a diet low in amino acids. Such a diet is indeed used in kidney disease, but for other reasons.

A great deal of research has been done all over the world. There is a great deal of data. What I am trying to do is put together the pieces of the jigsaw puzzle. Some pieces will be presented here. Argentine Research

Edmundo Fischer of Argentina reported the selective presence of a substance in the urine of schizophrenics. This substance behaved like bufotenin on paper chromatogrphy. Similar results were reported by Brune et al (1963).

British Research

Barrass et al (1970) reported a urine heteropeptide with a catecholamine residue, This appears to support American work by Friedhoff & van Winkle in 1962. The New York team found DMPEA, a catecholamine, to be present only in schizophrenics.

American Work
In 1965 Bergen of Massachusetts reported a toxic serum factor containing a small molecule. The small molecule had properties resembling a catecholamine. Again this supports the work of Friedhoff & van Winkle. In 1967 Creveling & Daly confirmed the presence of DMPEA in the "pink spot". The used mass spectrometry. However, they reported other substances in the "pink spot".

Conclusions

The "pink spot" has been confirmed all over the world. The British group Ridges & Bourdillon (1966) modified the intestinal flora with neomycin. This did not alter the "pink spot" on the chromatograms. This means that the spot was not due to intestinal bacteria. They found the "pink spot" only in schizophrenics. They found the pink spot in patients known not to have received any drug treatment. Thus the "pink spot" cannot be a drug artifact.
Their study was done using the double-blind technique. But this is only one of many theories. There is an obscure but plausible "rheomelanin" theory of Altschule & Hegedus (1973) of the US.
Another American, the late Linus Pauling, felt that alterations in blood-brain barrier permeability were possible. He felt that schizophrenia is genetic. Pauling was interested in "optimum molecular concentrations". Altschule at one time favored a toxic amine. He later changed his mind because melanins can accumulate in the body. It may be that both of Altschule's theories are correct. The accumulation of melanin could explain long term debilitation whereas the toxic amine could explain short term fluctuations. Greiner & Nicolson (1965) of Canada also favored the melanin theory.

Bibliography

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

2. www.associatedcontent.com/article/718067/an_endogenous_psychotogen_in_schizophrenia.html

3. www.associatedcontent.com/article/709479/moneydriven_medicine_vs_orthomolecular.html
4. www.associatedcontent.com/article/705601/the_alleviation_of_schizophrenia.html

5. www.associatedcontent.com/article/703807/why_orthomolecular_psychiatry.html