Schizophrenia is Organic

There have been numerous positive neuropathology reports in schizophrenia and related diseases. These reports prove Scientology to be wrong. Scientology has accused psychiatry of "junk science and bad medicine". They claim that there is no chemical imbalance. However, neuropathology data supports chemical imbalance theories. It is Scientology itself that is junk science.

South Africa

In 1975 Fisman of South Africa reported positive findings in the brain stem in "psychosis". He found ventricular dilation, atrophy, lipofuscin, glial knots, corpora amylacea, perivascular infiltration, necrosis, cell loss, calcification, neuronophagia, gliosis, sclerosis, iron encrustation, etc. A case with Huntington's chorea showed marked frontal atrophy and atrophy of the caudate nucleus. The patient had been suicidal. Lipofuscin was seen even though death was at 35 years of age. Gliosis and corpora amylacea were seen. Thus the neuropathology picture was similar to that seen in schizophrenia. After this study Fisman moved to Canada.

Germany

In 1897 and 1913 Alzheimer published articles on "dementia praecox". These articles were not about the disease that now bears his name. That was discussed in another article. Alzheimer reported cerebral lesions. The lesions and deficit were mainly in the second and third cortical layers. These were small-celled layers. The Vogts described alveolar degeneration, lipoid sclerosis, cellular ballooning, etc. This was reported by C. Vogt and O. Vogt in 1952.

France

Between 1904 and 1909 Klippel and Lhermitte published reports of cerebral lesions in "dementia praecox", which is now called "schizophrenia". They found progressive atrophy of the pyramidal cells of the fifth and sixth cortical layers with disappearance of Nissl bodies and of neurofibrils. Lipid deposits appeared in the cytoplasm. There was a marked reaction of the neuroglia. There was secondary degeneration of myelin related to the lesions of the pyramidal cells. There were similar lesions in the subcortical nuclei.

Italy

Buscaino reported racemose areas formed by metachromatic bodies in the cerebral cortex of schizophrenics. The myelin did not stain with the usual colorants. He attributed this to an abnormal amine (substance X).

United States

Scharenberg & Brown (1954) reported marked alterations in catatonia. They found extensive necrosis with marked reactions of the three types of glia. This appears to suggest an unknown toxic factor. This supports the toxin reported by Buscaino. Although Buscaino published many reports, one appeared in 1958.

Canada

Elvidge & Reed reported swelling of the oligodendroglia in both schizophrenia and manic-depressive psychosis. They found hypertrophy of astrocytes. They found a chronic process which suggested a toxic factor of metabolic origin. This was reported in 1938.

Mexico

Nieto & Escobar used Hortega's lithium-silver carbonate stain for neuroglial impregnation. They found glial prolifation in the diencephalon and mesencephalon. Unfortunately this does not tell us exactly what is happening, but it tells us where it is happening. In particular the hypothalamus was affected. The thalamus was also affected.

United Kingdom

Mott found atrophic changes in the hypophysis, an endocrine gland located in the base of the brain.

Conclusions

The whole picture is extremely complicated, unfortunately. However, there is a great deal of data, which is good. Making sense of this data is difficult but important. Kraepelin analyzed Alzheimer's data and compared it to the work of others in 1913. Kraepelin felt that it was valid. The disappearance of the Nissl bodies, reported by French workers and German workers, could be explained if amino acids were flooding the cells. This would also explain the lipid eposits reported by Klippel & Lhermitte. The gliosis reported by the Mexican workers and others supports a toxic factor theory. According to Buscaino, this toxic factor is an amine. Hopf reported lipofuscin deposits in 1952, which was a banner year for this type of research. The lipofuscin could either be a toxic factor itself or represent residue from the toxic amine or both. Amines can sometimes end up as neuromelanin (as in the case of dopamine), which looks like lipofuscin. It could be that an abnormal amine produces an abnormal type of neuromelanin. The abnormal amine could cause the cells to be floode with amino acids, explaining much of the data. If all of this is true, it would appear that a therapy could be a diet very low in amino acids. The Vogts found that the cellular structures slowly disintegrate. This probably means that the whole cell is affected. The first structure to go is the Nissl bodies, which house amino acids. The Mexican workers felt that stress was involved. They were probably correct. Stress might cause the release of the toxin.

References

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

2. www.associatedcontent.com/article/679607/world_research_on_schizophrenia.html
3. www.associatedcontent.com/article/671305/studying_schizophrenia_on_a_cellular.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

6. www.associatedcontent.com/article/644151/european_research_on_mental_health.html .