Schizophrenia as an Error in Evolution

Man has evolved to survive on a certain diet. This happened over many thousands of years. Our current diet is much different than the one we were designed by Mother Nature to survive on. Some might prefer the word "God" to "Mother Nature". The cave men didn't eat sugar, flour, or other processed foods. They didn't eat white rice. They didn't drink beer. They probably ate bananas and other fruits as well as vegetables. They probably ate a diet similar to that of apes and chimpanzees.

Our departure from the caveman diet may have contributed to chronic diseases such as schizophrenia, heart disease, cancer, hypertension, hemorrhoids, etc. Perhaps one of the few good things invented in food processing is the pasteurization of milk, named after Louis Pasteur.

Stress

Stress can occur in life. Bad things can happen. Unfortunately this stress may contribute to schizophrenia and other mental diseases.

Psychiatric Drugs

Unfortunately there are problems with psychiatric drugs. Sometimes these drugs are abused. The drugs have bad side effects. They can cause weight gain. Like other drugs, they could cause birth defects. One drug can interact with another. Drugs can interact with nutrients. This is also true of statins and other drugs, unfortunately.

Russian Research on Mental Illness

Doctor Natalia Uranova and doctor Diana Orlovskaya have consistently reported positive findings in schizophrenia. Decades ago Orlovskaya demonstrated a toxic factor in the blood which, when injected into animals, caused the blood glucose to go up. This suggests that the factor slows glucose metabolism. Similar results were reported by Savulev using a neuropathology assay on animals. After this, Orlovskaya switched over to neuropathology.

Russian Neuropathology Research

A 2001 report by Uranova et al revealed many clues to the biological mystery story of schizophrenia. They studied the prefrontal cortex and the striatum. These areas were studied in schizophrenia and bipolar disorder. The oligodendroglia can be satellites of neurons. These cells were studied by the Russian group using an electron microscope. Swollen cytoplasm and organelles were seen. The cytoplasm houses energy metabolism and protein synthesis. The mitochondria produce energy for the cell. Abnormalities were also seen in the nucleus.

Findings

Findings included hypertrophy of astrocytic processes, "reactive" oligodendroglial cells, cell swelling, pyknosis of nuclei, regressive changes, lysis of the nuclei, "cytoplasmic lipofuscin-like inclusions with lipid droplets", etc. An oligodendroglial cell was seen "lacking organelles". Abnormal inclusions were seen in the myelin sheaths of neurons.

The Pink Spot Theory of Schizophrenia

This theory is extensively discussed on my website, which is http://www.craigolson.bizhosting.com/. A large number of reports from all over the world have confirmed this controversial theory. It seems that the "pink spot" is only found on the chromatograms of the urine of schizophrenics. In 1971 Stanciu et al of Romania confirmed the theory. They reported the "significance and identification of 3,4-dimethoxyphenylethylamine in the urine of schizophrenic patients (pink spot reaction). This confirmed the original 1962 finding by Friedhoff and van Winkle.

German Work

In 1976 Zimmermann et al published another confirmatory study. They found no DMPEA in normal persons, but they did find it in schizophrenics. The original theory was proposed by Osmond, Smythies, and Harley-Mason in 1952.

More Russian Work

Russian work by Romasenko et al demonstrated an unknown toxic factor in the blood serum of schizophrenics. This strongly supports the DMPEA theory because the unknown toxic factor could be DMPEA (the "pink spot"). The Russians injected the blood serum of schizophrenics into white rats.
British Work

Work by Dr. Paul Averback of the United Kingdom, who later moved to Canada, demonstrated pathology in the brain in schizophrenia. The cells were autoflourescent. This signifies the presence of an abnormal autoflourescent substance. This substance was described by Averback as being "lipofuscin-like". This might be the end result of the DMPEA, which does not itself accumulate because it is unstable. Once the DMPEA is oxidized it might become stable. The location of Averback's lesions is suggestive. The lesions were located mostly in the basal ganglia, which are very high in dopamine. Dopamine is a precursor of DMPEA.

Ultimately the problem must be resolved on a molecular level. This was the view of the late Linus Pauling, who was correct. Although the evidence for this theory is strong, no current research is being done on it.

Conclusions

The Russian findings of abnormal mitochondria are consistent with an American report by Buchsbaum and Hazlett, who reported "abnormal glucose metabolism in schizophrenia" in 1998. This confirms Orlovskaya's earlier work in the Sixties. Glial cells are thought to affect neuron metabolism. Unfortunately the meaning of these findings is not completely clear. There are metabolic errors. The lipid droplets suggest that the cells may be over-eating. They are most likely not over-eating glucose because the glucose metabolism is too slow. The cells may be over-eating fat or amino acids. Excess amino acids would be converted to fat. This theory suggests that diet should be considered as a therapy. Perhaps the diet would be low in protein and fat. However, the Russian workers did not conclude this. The use of a diet was suggested by a brilliant Canadian doctor named "Gilka".

For more information, consult the bibliography. Many of my sources were obtained from a website called Pubmed. This is a US government website maintained by the National Library of Medicine of the US.

Bibliography

1. www.associatedcontent.com/article/723727/an_endogenous_inhibitor_of_monoamine.html
2. www.associatedcontent.com/article/722243/schizophrenia_an_error_in_homeostasis.html
3. www.associatedcontent.com/article/721845/phytochemicals_for_schizophrenia_cancer.html

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

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