Abnormal Psychology: The Etiology of Schizophrenia

"With the advent of neuroimaging techniques in the 1960s, it became possible to document what many had long suspected: that schizophrenia was associated with brain abnormalities. The earliest reports, based on computerized axial tomography, showed that patients had enlarged brain ventricles and especially increased volume of the lateral ventricles (Dennert & Andreasen 1983). As new imaging techniques were developed, these findings were replicated, and additional abnormalities were detected. (Henn & Braus 1999)." Walker, Elaine, Lisa Kestler, Annie Bollini and Karen M. Hochman

Introduction

The bibliography contains a great deal of background information on abnormal psychology in general and on schizophrenia and other mental diseases. Many different approaches have been used including genetics. According to citation #2 in the bibliography, schizophrenia is associated with a gene on chromosome 22q in location 11. This is the location where the enzyme COMT is coded. COMT is important in dopamine metabolism. It metabolizes dopamine into other substances. This appears to inactivate dopamine, but there is a strong theory that a toxic metabolite can be created.

The term "schizophrenia" was invented by the Swiss psychiatrist Bleuler in 1911.

Treatment

"The most common late-emerging syndrome is tardive dyskinesia (irregular twisting or writhing movements). The cause of these motor side effects is not established, but is assumed to be due to excessive dopamine D2 receptor blockade. The motor symptoms typically decline following the discontinuation of medication." Walker et al (2008)

Unfortunately treatment with drugs has been problematic.

"Drug-induced movement abnormalities are the main side effect associated with the typical antipsychotics. There are both early- and late-emerging motor side effects (Sadock & Sadock 2000). Early emerging "extrapyramidal" syndromes include pseudoparkinsonism (clinically similar to Parkinson's disease), dystonic reactions (sudden onset of sustained intense muscle contraction), and akathisia (restlessness)." Walker et al (see #1 in the Bibliography)

Progressive Brain Tissue Loss

Various studies have shown progressive brain tissue loss in schizophrenia including citation 5 in the bibliography. This proves the developmental theory to be false. Schizophrenia is a neurodegenerative disease.

Russian Research

"Electron microscopy revealed the prominent ulrastructural dystrophic and degenerative alterations of pericapillary oligodendrocytes in the prefrontal cortex in schizophrenic brains. The present study points out that the population of pericapillary oligodendrocytes is involved in the pathogenesis of schizophrenia. Damage and loss of pericapillary oligodendrocytes might lead to disruption of the blood-brain barrier and as a result to dysregulation of metabolic trafficking across the blood-brain barrier in the prefrontal cortex in schizophrenia." Vostrikov VM

My own theories are similar to those of Vostrikov. I believe that there is indeed an error in the blood-brain barrier. My theory is that tryptophan floods the brain cells in schizophrenia and also in depression. My own experiments support this. But what is to be done about this?

Food Allergy Theory

An orthomolecular scientist named Dr. Dohan first came up with a brain allergy theory for schizophrenia. This was based on the medical mimic called celiac disease. In celiac disease there are psychiatric symptoms as well as gastrointestinal symtoms. Dohan, of Philadelphia, thought that celiac disease provided an important clue to the etiology (causation) of schizophrenia. His work was greeted with some enthusiasm by orthomolecular scientists, but he was derided by orthodox psychiatrists. I believe that Dohan was partly right.

In celiac disease one amino acid, glutamine, is taken up too rapidly and poisons the brain. This is due to a problem in the alimentary canal. My view is that if one amino acid can do this, then others might be able to cause psychiatric symptoms as well. One of my experiments points towards tryptophan as the culprit in schizophrenia and depression. I do not wish to describe this experiment at this time because it is dangerous. If somebody with diabetes did the experiment on themselves, they could pass out. I knew that I did not have diabetes.

Conclusions

I have formulated what I call "Olson's Laws of Psychiatry". They are as follows:

1. Mental diseases are caused by disturbances in the brain metabolism of glucose. These disturbances slow the brain metabolism of glucose.

2. Any know physical disease such as hypoglycemia which slows the brain metabolism of glucose presents with psychiatric symptoms.

3. Disturbances of amino acid metabolism in which there is an excess of one or more amino acids in the brain can cause a slowing of brain glucose metabolism because the brain will burn the offending amino acid for fuel if it is glycogenic. A glycogenic amino acid can be converted to a carbohydrate intermediary. Tryptophan is glycogenic.

My proposed treatment for mental illness is a diet very low in tryptophan. This diet is complex because a lot of sugar can pump tryptophan into the brain by a complex mechanism involving insulin. Therefore carbohydrates must be restricted, but not banned. Some complex carbohydrates are essential. Sugar is banned.

Bibliography

1. Walker, Elaine, Lisa Kestler, Annie Bollini, and Karen M. Hochman. "Schizophrenia: etiology and course. " Annual Review of Psychology. 55 (Annual 2004): 401(30). Health Reference Center Academic. Gale. Needham Free Public Library. 6 Aug. 2008.2.

Bassett AS, Hodgkinson K, Chow EW, Correia S, Scutt LE, Weksberg R. 1998.22ql 1 deletion syndrome in adults with schizophrenia. Am. J. Med. Genet. 81(4):328-37.

3. Bleuler E. 1911. Group of Schizophrenias. Transl. J Zinkin, 1950. New York: Int. Univ. Press (From German).

4. Karayiorgou M, Morris MA, Morrow B. 1995. Schizophrenia susceptibility associated with interstitial deletions of chromosome 22q11. Proc. Natl. Acad. Sci. USA 92:7612-16.

5.

Rapoport JL, Giedd JN, Blumenthal J, Hamburger S, Jeffries N, et al. 1999. Progressive cortical change during adolescence in childhood-onset schizophrenia: a longitudinal magnetic resonance imaging study. Arch. Gen. Psychiatry 56(7):649-54.

6. www.associatedcontent.com/article/905903/the_human_brain_and_its_afflictions.html

7. http://www.associatedcontent.com/article/884197/back_barack.html

8. www.associatedcontent.com/article/868053/medical_mimics_of_schizophrenia.html

9. www.associatedcontent.com/article/851313/the_american_presidential_election.html
10. www.associatedcontent.com/article/846327/is_barack_obama_really_the_change_this.html
11. http://www.associatedcontent.com/article/833167/schizophrenia_is_caused_by_a_mescalinelike.html

12. Wang, H., S. Duan, J. Du, X. Li, Y. Xu, Z. Zhang, Y. Wang, G. Huang, G. Feng, and L. He. "Transmission disequilibrium test provides evidence of association between promoter polymorphisms in 22q11 gene DGCR14 and schizophrenia. " Journal of Neural Transmission. 113.10 (Oct 2006): 1551. Health Reference Center Academic. Gale. Needham Free Public Library. 6 Aug. 2008.

13. Vostrikov VM. [Decreased numerical density of pericapillary oligodendrocytes in the cortex in schizophrenia.] Zh Nevrol Psikhiatr Im S S Korsakova. 2007;107(12):58-65.