The Scientific Study of Schizophrenia and a Solution

I have written so many articles on psychiatry that I decided to use long titles so as not to repeat the same title.

Averback started his career in the United Kingdom. Then he moved to Canada. In 1981 he published a brilliant article in Archives of Neurology entitled "Lesions of the Nucleus Ansae Peduncularis in Human Neuropsychiatric Disease." It seems that the NAP cells were swollen. Averback's findings of fatty degeneration confirmed a century of previous work which he appears to have been unaware of.

Scioli (1909)

Scioli reported that the cells showed severe injury. Glia proliferation was seen in the molecular layer, the sixth layer, and medullary areas.

Cotton (1915)

In 1915 Cotton reported fatty deposits in "dementia praecox", which is now called "schizophrenia". He thought that this signified a toxin because he found similar fat deposits in alcoholics. He thought that schizophrenia was caused by an endogenous toxin.

Alzheimer (1897, 1913)

Unfortunately 1913 was the last year that Alzheimer published a report on "dementia praecox". He had already published a report on the disease that now bears his name. In schizophrenia Alzheimer found "severe grade sclerosis of ganglion cells with fatty degeneration signifies severe injury to function".

Bleuler (1915)

Even though Bleuler was a psychoanalyst, he believed that physical changes caused dementia praecox. Bleuler invented the term "schizophrenia". He believed that "some toxic action" caused dementia praecox.

Gurd (1920)

Gurd studied "nineteen cases of dementia praecox of unquestionable dagnosis". "In the Nissl's stain these nerve cells are pale: the chromatin is either entirely dissolved out of is present in the form of fine granules which appear equally throughout the whole cell body and are also evident in the dendrites." In other words, the Nissl bodies are being destroyed.

Acid Brain

A 2008 report claims that the pH of schizophrenic brains is too low (too acid). This is supposedly due to excess lactic acid in the brain. But where is the excess lactic acid coming from? The report did not answer that important question. The authors of this report were Nader D. Halim (a)(b), Barbara K. Lipska (c), Thomas M. Hyde (c), Amy Deep-Soboslay (c), E. Michael Saylor (c), Mary M. Herman (c), Jay Thakar (b), Ajay Verma (b), Joel E. Kleinman (c). See Ref. 2.

Author Affiliation:

(a) Graduate Program in Molecular and Cell Biology, Bethesda, MD 20814, USA

(b) Department of Neurology Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA

(c) Clinical Brain Disorders Branch, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health,10 Center Drive, Bethesda, MD 20892-1385, USA

A Theory

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.

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 lipofuchsin 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

The papers of Averback confirmed earlier reports of "structural lesions of the brain in young schizophrenics" in the words of Averback. The major new contributions of Averback were the locations of maximum pathology, which he located to the nucleus ansae penduclularis and the septal nuclei. The location of the septal area confirms earlier work by Robert Heath of Tulane University. The late Dr. Heath reported a toxic factor in the blood serum was causing electrical problems in the septal area. He called this toxic factor "taraxein". The "massive swollen neurons filled with lipid vacuolar and pigment material" reported by Averback appear to suggest that the neurons are over eating some macronutrients. The pigment could be a residue of the unknown toxin called "taraxein" by Heath. The destruction of the Nissl bodies observed by Cramer and Gurd appears to suggest that the macronutrients are amino acids. The Nissl bodies contain amino acids. If amino acids were flooding the cells, this would explain the swelling, the fat deposits, and the destruction of the Nissl bodies.

One would think that if all of this is true, a diet very low in amino acids should be tried as a therapy. The diet should also be low in fat because the cells appear to burst as a result of too much fat.

References

1. Alterations in kynurenine precursor and product levels in schizophrenia and bipolar disorder.(Report).Christine L. Miller, Ida C. Llenos, Mary Cwik, John Walkup and Serge Weis. Neurochemistry International52.6 (May 2008): p1297(7).

2. Increased lactate levels and reduced pH in postmortem brains of schizophrenics: Medication confounds.(Author abstract)(Report).Journal of Neuroscience Methods169.1 (March 30, 2008): p208(6).

3. www.associatedcontent.com/article/679899/the_molecular_and_cellular_pathology.html .

4. www.associatedcontent.com/article/669729/nutrition_against_cancer_and_mental.html .

5. www.associatedcontent.com/article/665637/american_research_on_mental_health.html .