A Review of Scientific Studies of Mental Disease

Perhaps the oldest scientific approach has been neuropathology. Averback's brilliant report in Archives of Neurology is available free full text at that journal's website.

"The nucleus of the ansa peduncularis in the substantia innominata frequently contains degenerating neurons in patients with Huntington's disease, Alzheimer's disease, schizophrenia, and possibly other neurological and neuropsychiatric conditions." Averback (1982)

See Ref. 1 for the citation. This article has greatly influenced my own theories. Clearly schizophrenia is organic. This means that Thomas Szasz, Peter Breggin, R. D. Laing, and other radicals are all wrong. Laing is deceased.

Averback (1982)

Averback wrote two brilliant articles that were similar in the same year, the other article dealing with the septal area. Averback found similar alterations in the septal area in young schizophrenics in the other study. This confirms Heath's 1954 electrophysiology studies localizing schizophrenia to the septal area using depth EEG electrodes.

The work discussed here was done at the Department of Pathology, University of Cambridge, Cambridge, England. Since then he moved to McGill University in Montreal.

"The cells show massive distention with solvent-extractable lipid-pigment vacuolar droplet material that imparts a distinctive light and electron microscopic appearance." Averback

In a subsequent article Averback blamed these findings on a virus. However, I feel that this was a mistake. I feel that the findings were due to a metabolic toxin. My view is that the fat droplets are caused by the cells overeating some macronutrients. I searched the article for a clue as to what the macronutrients were. I found one. He reported that the Nissl bodies were "barely recognizable". Since the Nissl bodies house amino acids, it because clear that amino acids were suspects.

But what is the pigment? Averback thought it was lipofuscin. This finding confirms Alzheimer's 1913 report of pigment in "dementia praecox". Lipofuscin is cellular garbage. This suggests an abnormal metabolic rate. The cell seems to be making garbage faster than the lysosomes can get rid of it. If amino acids were flooding the cells, this could cause an abnormal metabolic rate. Organelles could be destroyed. This would create cellular garbage.

Free Full Text Articles

There are a number of free full text articles that are available on the Internet. I have included some of my own in the references. These are on Associated Content. There are also many academic full text articles available at the journal sites including a 1999 one by Harrison in the journal Brain.

Amino Acids

Amino acids are found in protein. I have posted some photo albums at Gather. These are free. Some of these albums show the foods which contain various amino acids. One shows various foods high in protein. Protein is high in most animal products. My theory is that a low protein diet should be used to treat mental disease. Animal products should be avoided in this diet.

COMT

There is a genetic theory that the enzyme COMT is abnormal in schizophrenia. This is partly explained in Ref. 13 and 14. My theory is that a COMT inhibitor should be tried as a therapy because the enzyme COMT can create the toxin DMPEA from dopamine. DMPEA is only seen in schizophrenics and in the peyote cactus. Polyphenols are substances in food that are natural COMT inhibitors.

Conclusions

More research needs to be done. Some of the chemical errors have been discovered. Work needs to be done on new treatments. I favor the use of orthomolecular treatments. These are cheaper, safer, and more logical than drugs. The drugs have been largely trial & error with too many errors. More information is given in the references.

Buchsbaum and his colleagues have published a series of reports implicating slow brain glucose metabolism in schizophrenia. This is mostly in the frontal lobes and certain subcortical structures. The basal ganglia, which are high in dopamine, have been implicated.

References

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

2. Mettler FA: Anatomy of the basal ganglia, in Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology. Amsterdam, North Holland Publishing Co, 1968, pp 1-55.

3. Mettler FA: Neuroanatomy. St Louis, CV Mosby Co, 1948, pp 355-384.

4. Wolman M: Pigments in Pathology. New York, Academic Press Inc, 1969.

5. Torrey EF, Peterson MR: Schizophrenia and the limbic system. Lancet 1974;2:942-946.

6. Stevens JR: An anatomy of schizophrenia? Arch Gen Psychiatry 1973;29:177-189.

7. http://www.associatedcontent.com/article/1465561/advances_in_nutritional_science.html

8. Buchsbaum MS, Someya T, Teng CY, Abel L, Chin S, Najafi A, et al. PET and MRI of the thalamus in never-medicated patients with schizophrenia. Am J Psychiatry 1996; 153: 191-9.

9. Andreasen, N.C. Schizophrenia: The fundamental questions. Brain Res. Brain Res. Rev.31, 106-112 (2000).

10. Lewis, D.A., Lieberman, J.A. Catching up on schizophrenia: Natural history and neurobiology. Neuron28, 325-334 (2000).

11. Lieberman, J.A., Perkins, D., Belger, A., Chakos, M., Jarskog, F., Boteva, K., and Gilmore, J. The early stages of schizophrenia: Speculations on pathogenesis, pathophysiology, and therapeutic approaches. Biol. Psychiatry50, 884-897 (2001).

12. Maynard, T., Haskell, G., Lieberman, J., and LaMantia, A. 22q11 DS: Genomic mechanisms and gene function in DiGeorge/velocardiofacial syndrome. Int. J. Dev. Neurosci.20, 407-419 (2002).

13. Egan, M.F., Goldberg, T.E., Kolachana, B.S., Callicott, J.H., Mazzanti, C.M., Straub, R.E., Goldman, D., and Weinberger, D.R. Effect of COMT Val108/158Met genotype on frontal lobe function and risk for schizophrenia. Proc. Natl. Acad. Sci. U.S.A.98, 6917-6922 (2001).

14. Shifman, S., Bronstein, M., Sternfeld, M. et al. A highly significant association between a COMT haplotype and schizophrenia. Am. J. Hum. Genet.71, 1296-1302 (2002).

15. Gasparini, M., Fabrizio, E., Bonifati, V., and Meco, G. Cognitive improvement during tolcapone treatment in Parkinson's disease. J. Neural Transm.104, 887-894 (1997).

16. Malhotra, A.K., Pinals, D.A., Adler, C.M., Elman, I., Clifton, A., Pickar, D., and Breier, A.. Ketamine-induced exacerbation of psychotic symptoms and cognitive impairment in neuroleptic-free schizophrenics. Neuropsychopharmacology17, 141-150 (1997).

17. Sawa, A. and Snyder, S.H. Schizophrenia: Diverse approaches to a complex disease. Science296, 692-695 (2002).

18. www.associatedcontent.com/article/1424647/advances_in_world_psychiatry.html

19. www.associatedcontent.com/article/1457526/advances_in_orthomolecular_research.html

20. www.associatedcontent.com/article/1452386/amino_acids_why_all_the_fuss.html