Mental Health Science

"It is not ... that some people do not know what to do with truth when it is offered them, but the tragic fate is to reach, after patient search, a condition of mind-blindness, in which the truth is not recognized, though it stares you in the face." Sir William Osler, physician, 1849-1919

Introduction

This author has long suspected catecholamine-synthesizing enzymes in schizophrenia. One such enzyme is tyrosine hydroxylase. However, it would be dangerous to inhibit this enzyme, which produces L-dopa, because it could lead to a synthetic form of Parkinson's disease. DOPA is converted to dopamine, which is essential for the health of the brain. There is a methyl transferase enzyme which produces epinephrine from norepinephrine. The addition of the methyl group appears to make the compound very potent. Epinephrine may be involved in high blood pressure. In technical language high blood pressure is called "hypertension."

Stress

Stress is thought to induce "pathology", according to Weiss (1972). Dr. Julius Axelrod of NIMH has studied the catecholamine-controlling enzymes. Gray (1972) has suspected the limbic system of the brain. In particular Gray has suspected the septal area, the amygdala, the hippocampal area, the hypothalamus, etc.

Charcot

"We must not forget that psychology ... forms a part of medicine, and that it is after all, at least for the most part, nothing but the physiology of the higher portions of the brain." Charcot (1893)

Charcot was a teacher of Freud. Charcot was both a psychiatrist and a neurologist. Charcot studied "maladies" of the nervous system. Dr. Pierre Janet was also a student of Charcot. Korsakoff was a Russian doctor who had similar views. Thus Charcot (as well as Korsakoff, Wernicke, and others) believed in the "medical model". The "medical model" is accepted by orthomolecular doctors and scientists, but not by antipsychiatry radicals. The "medical model" is correct.

Newcomer

Dr. Newcomer is in fact a newcomer to this research. Newcomer feels that there are genetic factors in schizophrenia and in "delusional disorders". In fact there are a number of known genetic disorders which imitate schizophrenia including homocystinuria (an error in amino acid metabolism), Huntington's chorea, Alzheimer's disease, etc. Linus Pauling pointed out that a number of nutritional diseases (B12 deficiency, pellagra, etc.) imitate schizophrenia.

Hypercatabolism of Tryptophan

According to Ravikumar et al of India (2000), there is "hypercatabolism of tryptophan" in "neuropsychiatric disordrs". Tyrosine catabolism is also abnormal, but in a different way. "The concentration of tryptophan, quinolinic acid, kynurenic acid, serotonin, and 5-hydroxyindoleacetic acid was found to be higher in the plasma of patients with all these disorders ..." Free fatty acids were increased. Albumin was decreased. Digoxin, a modulator of amino acid transport, was "higher in these patients". Digoxin comes from the hypothalamus.

The article was published in Neurology India.

A Comprehensive Theory of Schizophrenia Based on Neuropathology Data

The theory is based on the work of a number of scientists including Sukhorukova of Russia. In 1969 it was called the Soviet Union. Since the collapse of the Soviet Union, many good things have happened, but there seems to have been reduced funding for medical research in Russia. In 1969 Sukhorukova reported a number of findings of "ultrastructural alterations in neural and glial elements". "Signs of intracellular edema", meaning swelling, were seen. Neuronal membranes and granules "were sometimes in a state of lysis".
Neuropathology Data
"Glial elements exhibited signs of edema and activation with glycogen accumulation in macroglial cells". The alterations were "chiefly in the neuronal synthesizing apparatus". "These alterations were possibly associated with changes in protein metabolism occurring in schizophrenia." Sukhoukova was correct. The synthesizing apparatus takes amino acids and uses them to make proteins. What Sukhorukova was unable to figure out was the fact that most of his data would be explained if too many amino acids were flooding the cells. This would cause the "activation" reported by Sukhorukova. It would also cause the increase in glycogen content reported by the Russian scientist. Pathology to the synaptic apparatus would be explained by an error in neurotransmitter metabolism, which could cause the flooding of the cell with amino acids. The destruction of membranal elements could be caused by a fat-soluble toxin which attacks the cell membrane. The granules resembling lipofuscin could represent either the toxin itself or a residue of the unknown toxin. Since dopamine forms neuromelanin, which looks much like lipofuscin, a toxic metabolite of dopamine could be the explanation of the lipofuscin.

Synthesis

Since the subjects of Sukhorukova were young, the lipofuscin was not due to aging. He claimed "a pathological process in nervous tissue". This is true, but it is vague. He noted that "the destruction of membranal and granular structures is especially prominent around lipofuscin granules". This could either indicate that the granules were cellular garbage, or that they were the cause of the problems. I have to believe that they are connected with the problem because cellular garbage would probably be cleaned up by processes in the organism if at all possible. The "simultaneous disruption of the synthesizing and energy apparatus of the cell" would be explained by a flooding of the cell with amino acids.

The treatment would probably be a very strict diet low in amino acids. Savulev published similar results in 1967 except that Savulev's experiments demonstrated a toxic factor in the "blood serum from schizophrenic patients". Savulev gave the serum to white rats. He found pathology in the mitochondria and tigroid substance of neurons in the cerebral cortex of the rats. He found the blood serum to be "neurotropic".

In 1952 Scharenberg and Brown of Michigan reported "histopathology of catatonic states". This is nothing new, since Alzheimer and others had previously reported pathology in "dementia praecox". Thus there has been a very long history of positive findings.

Conclusions

Newcomer, in his assessment of the etiology and pathophysiology of schizophrenia, pointed out the similarity of schizophrenic symptoms to those from certain drug intoxications. These included PCP, ketamine, amphetamines, L-dopa, etc. This is probably not by chance. There may be an internal chemical similar to amphetamine that causes schizophrenia. Amphetamine is very similar to dopamine in struture. Thus an abnormal metabolite of dopamine may be the culprit.

But what do we do about it? Drugs have been plagued by side effects. The approach of a diet very low in amino acids is advocated at my website, which is http://www.craigolson.bizhosting.com/. The rationale is that the toxic factor is causing amino acids to flood the brain cells. This in turn causes a slowing of brain glucose metabolism, much like a cerebral diabetes. It is the slowing of brain glucose metabolism that causes the symptoms. The brain relys on glucose for energy.

Bibliography

1. www.associatedcontent.com/article/748865/schizophrenia_as_an_encephalopathy.html

2. www.associatedcontent.com/article/739945/new_ideas_in_psychiatry.html