The Neurochemistry of Mental Diseases

The temporal lobes have long been suspected in psychosis because psychosis is often seen in temporal lobe epilepsy. Also neuropathology has been reported in the temporal lobes in schizophrenia. However, pathology has also been reported in the frontal lobes, the brain stem, the limbic area, etc. Fisman (1975) reported glial nodules (gliosis) in the brain stem of schizophrenics. He suspected a virus.

Fisman (1975)

"An unexpected finding in this study was the
presence of glial nodules and perivascular
infiltration in 6 of the 7 patients with schizophreniform features and no other evidence of
cerebral disease." Fisman (1975)

Later (1993) Bloom favored a neurodevelopmental origin of schizophrenia. However, this theory is incompatible with gliosis. Gliosis signifies a toxic factor or virus.

Daniel H. Mathalon, PhD, MD; Edith V. Sullivan, PhD; Kelvin O. Lim, MD; Adolf Pfefferbaum, MD

This group found progressive brain volume decline is schizophrenia, killing the popular but false neurodevelopmental theory. See Ref. 24. This fairly recent study was done in 2001.

Stevens (1982)

Stevens pounded more nails into the coffin of the neurodevelopmental theory. She found subcortical gliosis, which signifies either a toxic factor or a virus. Gliosis is seen in toxic diseases and virus diseases. Stevens also reported corpora amylacea, which are starch bodies seen in errors of glucose metabolism. This indicates that schizophrenia is an error of brain glucose metabolism in which glucose is being burned too slowly.

The finding of gliosis means that schizophrenia is a neurodegenerative disease cause by a toxic factor or factors. See. Ref. 7.

Alzheimer (1897)

In a series of brilliant papers on "dementia praecox" from 1897 to 1913, shortly before his death, Alzheimer reported microscopic brain lesions in this disease. He found ameboid glia (gliosis), fatty degeneration, pigment deposits, cell loss, etc. in the cortex. In my opnion the fat deposits came from excessive amino acids flooding the cells. This also explains the cell loss. It also explains the corpora amylacea described by Stevens. The brain is burning amino acids instead of glucose.

Vogt & Vogt (1952)

These brilliant German neuropathologists found alterations in all cases of schizophrenia including fat vacuoles, lipofuscin, tigrolysis, cell death, etc. Tigrolysis means the destruction of the Nissl bodies, which contain amino acids. This is explained by my theory of amino acids flooding the cells. Lipofuscin is cellular garbage. Lipofuscin would be explained by an increased cellular metabolic rate. This increased rate could also be explained by amino acids flooding the brain cells. The Vogts reported subcortical pathology.

Conclusions

I have included a lot of academic references here because there are people who are skeptical of my theories. I have based my theories on over a century of data. But what are the treatments? Unfortunately there have been many problems with psychiatric drugs. See references 15, 16, and 18. These drugs are very expensive, and often the taxpayers pay for them.

My suggestion is orthomolecular treatments which are cheaper, safer, and more logical. Since amino acids are flooding the brain cells, a diet very low in protein is suggested. This diet would be high in fiber, which is beneficial.

Another theory I have is that polyphenols, including flavonoids, may help. These substances inhibit the enzyme COMT which creates DMPEA. DMPEA is a toxin that is found only in schizophrenics and in the peyote cactus. Flavonoids are plant pigments, and they are found only in plant foods such as tea, citrus fruits, berries, etc. I plan to write more on flavonoids in the future.

References

1.

The neuropathological effects of antipsychotic drugs.

Harrison PJ.

Schizophr Res. 1999 Nov 30;40(2):87-99. Review.

2.

The neuropathology of schizophrenia. A critical review of the data and their interpretation.

Harrison PJ.

Brain. 1999 Apr;122 ( Pt 4):593-624. Review.

3. Corsellis JAN. Psychoses of obscure pathology. In: Blackwood W, Corsellis JAN, editors. Greenfield's neuropathology. 3rd ed. London: Edward Arnold; 1976. p. 903-15.

4. David GB. The pathological anatomy of the schizophrenias. In: Richter D, editor. Schizophrenia: somatic aspects. London: Pergamon Press; 1957. p. 93-130.

5. David AS, Cutting JC. The neuropsychology of schizophrenia. Hove (UK): Lawrence Erlbaum; 1994.

6. Fisman M. The brain stem in psychosis. Br J Psychiatry 1975; 126: 414-22.

7. J. R. Stevens
Neuropathology of Schizophrenia
Arch Gen Psychiatry, October 1, 1982; 39(10): 1131 - 1139.

8. Meyer, A. (1971) Psychoses of obscure pathology. In
Greenfield's Neuropathology (ed. W. Blackwood).
London.

9. Bleuler E. Dementia praecox or the group of schizophrenias 1911. Transl. J. Zinkin. New York: International Universities Press; 1950.

10. Bloom FE. Advancing a neurodevelopmental origin for schizophrenia. [Review]. Arch Gen Psychiatry 1993; 50: 224-7.

11. www.associatedcontent.com/user/50445/craig_olson.html

12. http://www.associatedcontent.com/article/1395958/relationship_between_bipolar_disorder.html

13. www.associatedcontent.com/article/1485724/a_hypothesis_for_mental_disease.html

14. www.associatedcontent.com/article/1496620/mental_illness_perspectives_including.html

15.

Aasly J, Sando S, Undeland M, Waage A.

Tidsskr Nor Laegeforen. 2009 Jan 1;129(1):33-5. Norwegian.

16.

Atypical antipsychotic drugs and the risk of sudden cardiac death.

Ray WA, Chung CP, Murray KT, Hall K, Stein CM.

N Engl J Med. 2009 Jan 15;360(3):225-35.

17. Averback P. Lesions of the nucleus ansae peduncularis in neuropsychiatric disease. Arch Neurol 1981; 38: 230-5.

18. Jellinger K. Neuropathologic findings after neuroleptic long-term therapy. In: Roizin L, Shiraki H, Grcevic N, editors. Neurotoxicology. New York: Raven Press; 1977. p. 25-42.

19. Jellinger K. Neuromorphological background of pathochemical studies in major psychoses. In: Beckmann H, Riederer P, editors. Pathochemical markers in major psychoses. Berlin: Springer; 1985. p. 1-23.

20. Miyakawa T, Sumiyoshi S, Deshimaru M, Suzuki T, Tomonari H. Electron microscopic study on schizophrenia. Mechanism of pathological changes. Acta Neuropathol (Berl) 1972; 20: 67-77.

21. Miyake T, Kitamura T, Takamatsu T, Fujita S. A quantitative analysis of human astrocytosis. Acta Neuropathol (Berl) 1988; 75: 535-7.

22. Nieto D, Escobar A. Major psychoses. In: Minckler J, editor. Pathology of the nervous system. New York: McGraw-Hill; 1972. p. 2655-65.

23. www.associatedcontent.com/article/1506969/a_review_of_scientific_studies_of_mental.html

24. Progressive Brain Volume Changes and the Clinical Course of Schizophrenia in Men: A Longitudinal Magnetic Resonance Imaging Study
Mathalon et al.
Arch Gen Psychiatry 2001;58:148-157.

25. Progression of Brain Volume Changes in Adolescent-Onset Psychosis
Reig et al.
Schizophr Bull 2009;35:233-243.

26. Excessive Brain Volume Loss Over Time in Cannabis-Using First-Episode Schizophrenia Patients
Rais et al.
Am. J. Psychiatry 2008;165:490-496.

27. The Concept of Progressive Brain Change in Schizophrenia: Implications for Understanding Schizophrenia
DeLisi
Schizophr Bull 2008;34:312-321.

28. What Happens After the First Episode? A Review of Progressive Brain Changes in Chronically Ill Patients With Schizophrenia
Hulshoff Pol and Kahn
Schizophr Bull 2008;34:354-366.

29. Progressive Brain Volume Loss During Adolescence in Childhood-Onset Schizophrenia
Sporn et al.
Am. J. Psychiatry 2003;160:2181-2189.

30. Progressive Structural Brain Abnormalities and Their Relationship to Clinical Outcome: A Longitudinal Magnetic Resonance Imaging Study Early in Schizophrenia
Ho et al.
Arch Gen Psychiatry 2003;60:585-594.

31. Progressive Decrease of Left Superior Temporal Gyrus Gray Matter Volume in Patients With First-Episode Schizophrenia
Kasai et al.
Am. J. Psychiatry 2003;160:156-164.

32. Alzheimer A: Beiträge zur pathologischen Anatomie der Hirnrinde und zur anatomischen Grundlage einiger Psychosen. Monatsschr Psychiatr Neurol 1897;2:82-119.

33. Kraepelin E: Dementia Praecox and Paraphrenia. Edinburgh, E & S Livingstone, 1919.

34. Buscaino VM: Le cause anatomo-patologiche della manifestazione schizofrenica nella demenza precoce. Riv Patol Nerv Ment 1920;25:197-226.

35. Josephy H: Dementia praecox (Schizophrenie), in Bumke O (ed): Die Anatomie der Psychosen. Berlin, Springer Verlag, 1930, p 763.

36. Spielmeyer W: The problem of the anatomy of schizophrenia. Res Publ Assoc Res Nerv Ment Dis 1931;10:105-110.

37. Vogt C, Vogt O: Alterations anatomiques de la schizophrenia et d'autres psychoses dites fonctionelles, in Proceedings of the First International Congress of Neuropathology. Turin, Italy, Rosenberg & Sellier, 1952, vol 1, pp 515-532.

38. Bruetsch WL: Specific structural neuropathology of the central nervous system (rheumatic, demyelinating, vasofunctional, etc) in schizophrenia, in Proceedings of the First International Congress of Neuropathology. Turin, Italy, Rosenberg & Sellier, 1952, vol 1, pp 487-499.

39. Tatetsu S: On histologie findings in schizophrenia and schizophrenic state, in Mitsuda H, Fukuda T (eds): Biological Mechanisms of Schizophrenia and Schizophrenia-like Psychoses. Tokyo, Igaku-Shoin Ltd, 1974, pp 288-289.