Brain Abnormalities in Mental Diseases

"On the one hand, cannabis is the most widely used illegal drug. There is substantial evidence that cannabis has to be classified as an independent risk factor for psychosis that may lead to a worse outcome of the disease. This risk seems to be increased in genetically predisposed people and may depend on the amount of cannabis used."

Müller-Vahl KR, Emrich HM (2008) Ref. 3.

Introduction

For many years scientists have searched for biological markers in the various forms of mental disease. Many putative biological markers have been found, only to be attacked by skeptics. My view is that the skeptics can and have been wrong many times. Some reviewers have had a negative bias. They blindly accept all negative findings and question all positive findings.

Biological Markers

"The initial prodromal state of psychosis (IPS) is defined as an early disease stage prior to the onset of overt psychosis characterized by sub-threshold or more unspecific psychiatric symptoms. Little is known regarding the biochemical changes during this period." Huang et al (2007) #5

I included this quote to explain what the word "prodomal" means.

"The key metabolic changes included elevated glucose levels, reduced lactate and acetate levels and a decrease in pH." Huang et al (2007)

This group is from the UK. They studied the cerebrospinal fluid of schizophrenics. Their article is available free full text on the Internet. Simply go to their article on Pubmed, which provides the link. My articles are also available free full text on the Internet (#9).

Psychiatric Drugs

Unfortunately drugs not only make research difficult, but they also have been plagued with bad side effects (see #14). They can kill off some of your blood cells, which can be very dangerous.

Macht (1949)

Macht of England reported an unknown toxic factor in the blood of schizophrenics using plant growth as an assay. The plants with the serum from schizophrenics did not grow well.

Hempel & Treff (1959)

This group found increased glial cell density (gliosis) in the thalamus of schizophrenics, but reduced neuronal density (-44%). This indicates brain cell loss.

Fungfeld (1954)

Fungfeld found changes in brain cells in schizophrenia. "Schwundzellen" were reported. These were abnormal cells. This was also reported by Baumer in 1954.

Fungfeld found changes in the Nissl-stained cytoplasmic material (Nissl bodies) in 7 0f 8 cases of catatonia.

Baumer (1954)

Baumer found cell loss.

Romasenko (1967)

Romasenko of Moscow injected serum from schizophrenics into rats. The brains of the rats were then examined. Degenerative changes were seen in the mitochondria. This kills the popular but false neurodevelopmental theory of schizophrenia. It proves the presence of an unknown toxic factor in the blood serum. It supports earlier work by Heath of New Orleans, who discovered "taraxein", a toxic blood globulin found only in schizophrenics. The Russian work and Heath's work both support neurodegenerative theories.

Snezhnevsky & Vartanyan (1971)

These two brilliant Russian scientists reported an "erythrolytic action of schizophrenic serum" seen with the electron microscope. They incubated red blood cells in the serum of schizophrenics. This caused hemolysis (destruction of cells). The Russians reported their toxic factor to be a beta globulin. The Russians also reported abnormal lymphocytes.

Averback (1981a, 1981b)

Work by Averback in 1981 reported severe pathology in both the septal area and the nucleus ansae peduncularis. Averback found massive bloating and death of neurson, which were filled with fat.

Casanova et al

This group, including Manuel Casanova and Janice Stevens, published a report in the book "New Biological Vistas in Schizophrenia". It seems that an inferior technique for finding gliosis is being used. This inferior technique gives false negative results. It fails to detect moderate gliosis. The Holzer stain was reported to be a better technique.

The false negative reports on gliosis have fooled even the famous Dr. Harrison of Oxford, an otherwise brilliant neuropathologist.

Conclusions

The fat deposits reported by Alzheimer, Averback, the Vogts, and others suggest that the brain cells may be overeating in schizophrenia. This could be caused by an error in the blood-brain barrier. The destruction of the Nissl bodies, which house amino acids, suggests that amino acids may be the culprits. If amino acids are indeed flooding the brain cells and the blood cells, than this would explain the hemolysis observed by Russian scientists.

All of this suggests a diet very low in amino acids as a rational treatment. All too often psychiatric treatments are trail & error with far too many errors.

References

1.Relationship of cerebrospinal fluid glucose metabolites to MRI deep white matter hyperintensities and treatment resistance in bipolar disorder patients.

Regenold WT, Hisley KC, Phatak P, Marano CM, Obuchowski A, Lefkowitz DM, Sassan A, Ohri S, Phillips TL, Dosanjh N, Conley RR, Gullapalli R.

Bipolar Disord. 2008 Nov;10(7):753-64.

2.Morphometric Brain Abnormalities in Schizophrenia in a Population-Based Sample: Relationship to Duration of Illness.

Tanskanen P, Ridler K, Murray GK, Haapea M, Veijola JM, Jääskeläinen E, Miettunen J, Jones PB, Bullmore ET, Isohanni MK.

Schizophr Bull. 2008 Nov 17.

3.Cannabis and schizophrenia: towards a cannabinoid hypothesis of schizophrenia.

Müller-Vahl KR, Emrich HM.

Expert Rev Neurother. 2008 Jul;8(7):1037-48.

4.Cerebrospinal fluid: identification of diagnostic markers for schizophrenia.

Schwarz E, Bahn S.

Expert Rev Mol Diagn. 2008 Mar;8(2):209-16.

5.CSF metabolic and proteomic profiles in patients prodromal for psychosis.

Huang JT, Leweke FM, Tsang TM, Koethe D, Kranaster L, Gerth CW, Gross S, Schreiber D, Ruhrmann S, Schultze-Lutter F, Klosterkötter J, Holmes E, Bahn S.

PLoS ONE. 2007 Aug 22;2(1):e756.

6. Yung AR, McGorry PD (1996) The prodromal phase of first-episode psychosis: past and current conceptualizations. Schizophr Bull 22: 353-370.

7. Huang JT, Leweke FM, Oxley D, Wang L, Harris N, et al. (2006) Disease biomarkers in cerebrospinal fluid of patients with first-onset psychosis. PLoS Med 3: e428.

8. Holmes E, Tsang TM, Huang JT, Leweke FM, Koethe D, et al. (2006) Metabolic profiling of CSF: evidence that early intervention may impact on disease progression and outcome in schizophrenia. PLoS Med 3: e327.

9. http://www.associatedcontent.com/article/1288595/new_hope_for_the_terrible_diseases.html

10. www.associatedcontent.com/article/1292687/healing_schizophrenia.html

11. Fernandes J, Berger R, Smit GP (1982) Lactate as energy source for brain in glucose-6-phosphatase deficient child. Lancet 1: 113.

12.[Proteomics: biomarker research in psychiatry]

Hünnerkopf R, Grassl J, Thome J.

Fortschr Neurol Psychiatr. 2007 Oct;75(10):579-86. Epub 2007 Jun 13. Review. German.

13.CSF biomarker discovery using label-free nano-LC-MS based proteomic profiling: technical aspects.

Huang JT, McKenna T, Hughes C, Leweke FM, Schwarz E, Bahn S.

J Sep Sci. 2007 Feb;30(2):214-25.

14.Prevention of clozapine-induced granulocytopenia/agranulocytosis with granulocyte-colony stimulating factor (G-CSF) in an intellectually disabled patient with schizophrenia.

Rajagopal G, Graham JG, Haut FF.

J Intellect Disabil Res. 2007 Jan;51(Pt 1):82-5.

15.

Profiling of CSF: small subgroups.

Hambridge D.

PLoS Med. 2006 Oct;3(10):e470; author reply e468.