Concepts of Schizophrenia

I have an important subtheory of the theory of evolution. My subtheory is that many diseases are errors in evolution. I'm sure somebody has thought of this before, but I have not seen it in writing. Brain diseases are examples. Some brain diseases are caused by trauma, but most aren't. Schizophrenia may be an error in evolution. Multiple sclerosis may be an error in evolution. On the other hand, post-traumatic stress disorder (PTSD) is considered environmental. But there could be an inherited weakness in the person's ability to cope with stress.

The Neurodevelopmental Theory Is False

Many studies, including Ref. 4, have shown "progressive brain structural change" in schizophrenia. This means that schizophrenia is a neurodegenerative disease. A neurodevelopmental disease would not show this. There is progressive tissue loss.

Amphetamine

Once used as a medicine, amphetamine is now largely (except for Ritalin) used as a drug of abuse. Ritalin, given to children, is an amphetamine analog (methylphenidate). Other amphetamine analogs are notorious drugs of abuse (including "Ecstacy"). Ref. 8 documents the fact that amphetamine causes dopamine release. Since amphetamine psychosis imitates schizophrenia, this suggests that dopamine may produce a metabolite that is toxic like amphetamine. Schizophrenia may be caused by a toxic dopamine metabolite or metabolites.

This theory is popular in Japan, where there was a terrible epidemic of methamphetamine abuse.

Brain Tissue Loss

Ref. 13 through 18 have all documented brain tissue loss in schizophrenia. What does this mean? It means that schizophrenia is a neurodegenerative disorder as declared by Kraepelin in 1919. It means that schizophrenia is organic. However, knowing this is not enough. We need to find out what is killing the cells.

Drugs

Unfortunately psychiatric drugs can cause tardive dyskinesia, dystonia, and other problems (see Refs. 20 and 21).

Dopamine

The dopamine hypothesis has been one of the main theories for schizophrenia. The fact that psychiatric drugs act on dopamine is why we see Parkinsonian side effects. But what is the best treatment? My view is that orthomolecular treatment is the way to go. It is more rational, cheaper, and safer than drugs. Psychiatry has gone with the drugs because there is more money to be made in this approach. What we have is money-driven medicine.

Conclusions

Ref. 24 is an example of orthomolecular treatment. My own ideas are different than those of Hoffer, although I agree that orthomolecular treatment is the way to go. I favor a diet high in flavonoids and low in protein. Ref. 1 and Ref. 2 explains the rationale for this. These articles are available free full text at Associated Content. I also favor the use of fiber supplements.

References

1. www.associatedcontent.com/article/1593193/amino_acids_in_psychiatry.html

2. www.associatedcontent.com/article/1542115/superfoods_and_supplements.html

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

4. DeLisi LE, Sakuma M, Tew W, Kushner M, Hoff AL, Grimson R. Schizophrenia as a chronic active brain process: a study of progressive brain structural change subsequent to the onset of schizophrenia. Psychiatry Res 1997a; 74: 129-40.

5. P. J. Harrison
The neuropathology of schizophrenia: A critical review of the data and their interpretation
Brain, April 1, 1999; 122(4): 593 - 624.

6. P. J HARRISON
Schizophrenia neuropathology: tortoises and hares
J. Neurol. Neurosurg. Psychiatry, October 1, 1998; 65(4): 432 - 432.

7. Jacobsen LK, Giedd JN, Castellanos FX, Vaituzis AC, Hamburger SD, Kumra S, et al. Progressive reduction of temporal lobe structures in childhood-onset schizophrenia. Am J Psychiatry 1998; 155: 678-85.

8. Laruelle M, Abi-Dargham A, van Dyck CH, Gil R, D'Souza CD, Erdos J, et al. Single photon emission computerized tomography imaging of amphetamine-induced dopamine release in drug-free schizophrenic subjects. Proc Natl Acad Sci USA 1996; 93: 9235-40.

9. 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.

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

11. Plum F. Prospects for research on schizophrenia. 3. Neurophysiology. Neuropathological findings. Neurosci Res Program Bull 1972; 10: 384-8.

12. Roberts GW. Schizophrenia: a neuropathological perspective. [Review]. Br J Psychiatry 1991; 158: 8-17.

13. A. L. Sporn, D. K. Greenstein, N. Gogtay, N. O. Jeffries, M. Lenane, P. Gochman, L. S. Clasen, J. Blumenthal, J. N. Giedd, and J. L. Rapoport
Progressive Brain Volume Loss During Adolescence in Childhood-Onset Schizophrenia
Am J Psychiatry, December 1, 2003; 160(12): 2181 - 2189.

14. B.-C. Ho, N. C. Andreasen, P. Nopoulos, S. Arndt, V. Magnotta, and M. Flaum
Progressive Structural Brain Abnormalities and Their Relationship to Clinical Outcome: A Longitudinal Magnetic Resonance Imaging Study Early in Schizophrenia
Arch Gen Psychiatry, June 1, 2003; 60(6): 585 - 594.

15. Falkai P, Bogerts B (1986) Cell loss in the hippocampus of schizophrenics. Eur Arch Psychiat Neurol Sci 236:154-161.

16. Lim KO, Sullivan EV, Zipursky RB, Pfefferbaum A (1996) Cortical gray matter volume deficits in schizophrenia: a replication. Schizophr Res 20:157-164.

17. Nelson MD, Saykin AJ, Flashman LA, Riordan HJ (1998) Hippocampal volume reduction in schizophrenia as assessed by magnetic resonance imaging. Arch Gen Psychiat 55:433-440.

18. Schlaepfer TE, Harris GJ, Tien AY, Peng LW, Lee S, Federman EB, Chase GA, Barta PE, Pearlson GD (1994) Decreased regional cortical gray matter volume in schizophrenia. Am J Psychiat 151:842-848.

19. Zipursky RB, Lim KO, Sullivan EV, Brown BW, Pfefferbaum A (1992) Widespread cerebral gray matter volume deficits in schizophrenia. Arch Gen Psychiat 49:195-205.

20.

Successful treatment of tardive lingual dystonia with botulinum toxin: case report and review of the literature.

Hennings JM, Krause E, Bötzel K, Wetter TC.

Prog Neuropsychopharmacol Biol Psychiatry. 2008 Jul 1;32(5):1167-71. Epub 2007 Sep 18. Review.

21.

Clozapine-induced hypersalivation: a review of treatment strategies.

Sockalingam S, Shammi C, Remington G.

Can J Psychiatry. 2007 Jun;52(6):377-84. Review.

22.

The future of psychiatry as clinical neuroscience.

Reynolds CF 3rd, Lewis DA, Detre T, Schatzberg AF, Kupfer DJ.

Acad Med. 2009 Apr;84(4):446-50.

23.

Contribution of leptin to the formation of neuroleptic obesity in patients with schizophrenia during antipsychotic therapy.

Gorobets LN.

Bull Exp Biol Med. 2008 Sep;146(3):348-50.

24.

Successful treatment of schizophrenia requires optimal daily doses of vitamin B3.

Hoffer A, Prousky J.

Altern Med Rev. 2008 Dec;13(4):287-91.