A Hypothesis for Mental Disease

"Learn, compare, collect the facts."
Ivan Pavlov

"How much easier it is to be critical than to be correct."
Benjamin Disraeli

Introduction

Mental illness is a diabetes of the brain. In diabetes mellitus the blood sugar is high. In mental illness the cerebrospinal fluid glucose is high. This has been measured in schizophrenia by Holmes et al. (Ref. 12). Abnormal glucose tolerance tests have been reported in both schizophrenia and in depression. The blood glucose gets too high after a load of glucose.

But why does this happen? The reason is that the brain is burning amino acids instead of glucose in mental diseases. This is what causes the symptoms.

Elaine Holmes

Holmes is from the Dept. of Biological Chemistry, Biomedical Sciences Division, Faculty of Medicine, Imperial College, London, United Kingdom. Holmes and her group also found the pH to be low in the cerebrospinal fluid of drug-naive schizophrenics. The rise in glucose of the drug-naive schizophrenics was localized to the brain. It was high in the CSF, but not in the serum. The low pH could be due to excess lactic acid. This is seen in mitochondrial impairments.

Neurohistopathology

In 1913 Alois Alzheimer published a brilliant report on the neurohistopathology of "dementia praecox". Unfortunately this paper appears to have never been translated into English. Both Alzheimer and Wernicke reported neuropathology findings in the various forms of mental disease. Alzheimer reported the positive findings in 55 cases of dementia praecox. He found gliosis, lipid degeneration, and other findings. These were most pronouced in the second and third layers of the cerebral cortex.

In 1933 Elvidge & Reed studied biopsies from schizophrenics and from patients with manic-depressive psychosis. They found swelling of oligodendroglial cells in both types of patients. Similar findings have been reported more recently postmortem by Russian scientists. Elvidge & Reed also reported hyperetrophy of astrocytes. This was most pronouced in the subcortical white matter. They hypothesized that their findings resulted from toxic metabolic factors.

In 1952 the Vogts reported numerous changes in 35 brains studied by serial section.

Macrostructure

In 1927 two German scientists, Jacobi & Winkler, reported altered brain macrostructure. They found enlarged ventricles using pneumoencephalography, an old technique.

Metabolic Disorder

In 1935 Gjessing reported a metabolic disorder in periodic catatonia. There was abnormal nitrogen metabolism. Later in 1957 Heath reported an abnormal protein in the blood of schizophrenics.

Electrophysiological Dysfunction

In 1954 Heath reported abnormal depth EEGs in the septal area of the brain in schizophrenia. This is a subcortical structure in the limbic system.

Disastrous Treatments

Unfortunately many of the organic treaztments were disastrous. This included chemical convulsions induced by von Meduna of Hungary in 1935. This was the first type of shock treatment. Insulin coma was introduced in 1936 by Sakel & Dussik. It was later abandoned, fortunately. There were deaths with this treatment.

Psychosurgery was introduced by Moniz in 1936.

Biochemical Treatment

Megavitamin treatment was introduced by Hoffer et al in 1957. This influenced Pauling, who introduced "orthomolecular" psychiatry in a brilliant 1968 paper in the journal Science.

Neuroleptics were started by Delay and Deniker in 1952. This was called "pharmacotherapy".

Kety

In two similar papers in 1959 and 1960, Kety rejected the carbohydrate theory because his research found that the brain oxygen consumption was normal in schizophrenia. Kety was a professor of Harvard Medical School. However, Kety was proven wrong by Dr. Carol Tamminga and her group in 1992. It seems that Kety did not consider the possibility that the brain was burning something else instead of glucose. In my theory the brain is burning amino acids instead of glucose, resulting in normal oxygen consumption but abnormal energy (ATP) production. Tamminga et al used the PET (positron emission tomography technique. They found a remarkable reduction in glucose metabolism in the medial temporal structures. This area is also called the parahippocampal gyrus.

The work by Tamminga et al (1992) was done of "drug-free" individuals. In 1997 it was discussed in the textbook called "The American Psychiatric Press Textbook of Neuropsychiatry", edited by Yudofsky & Hales.

Conclusions

"No twisted thought without a twisted molecule ..." Ralph Gerard

There is a toxic factor in the blood that causes these metabolic changes. More research needs to be done. However, at this point it would appear that a diet very low in amino acids might help because these amino acids are flooding the brain cells. More information is given in the references. Some graphics are given in my photo albums published on Gather. The protein contents of food and the various amino acids in foods are shown.

Also more information is given in my previous articles on Associated Content which are given free full text. Some of these are in the references. Some of the adverse side effects of psychiatric drugs, some of which can cause physical addiction, are given in the references. Depakote, an epilepsy drug, is now being used as a mood stabilizer, even though the FDA never approved it for that purpose. Doctors can do that. Unfortunately abrupt withdrawal can result in seizures.

References

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

8. www.associatedcontent.com/article/1395958/relationship_between_bipolar_disorder.html

9. Raskind, Murray A. "Diagnosis and treatment of depression comorbid with neurologic disorders.(Author abstract)." American Journal of Medicine 121.11 (Nov 2008): S28-S37. Health Reference Center Academic. Gale. Watertown Public Library. 12 Feb. 2009
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10. Tandon, Rajiv, Matcheri S. Keshavan, and Henry A. Nasrallah. "Schizophrenia, 'Just the Facts' What we know in 2008. 2. Epidemiology and etiology.(Report)." Schizophrenia Research 102.1-3 (July 2008): 1(18). Health Reference Center Academic. Gale. Watertown Public Library. 12 Feb. 2009
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11. Regenold WT, Phatak P, Kling MA, Hauser P (2004) Post-mortem evidence from human brain tissue of disturbed glucose metabolism in mood and psychotic disorders. Mol Psychiatry 9: 731-733.

12. Holmes E, Tsang TM, Huang JTJ, 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(8): e327. DOI: 10.1371/journal. pmed.0030327

13. Hoffer, Abram & Osmond, Humphry (1952) Paper to Dementia Praecox Committee, Scottish Rites Masons, New York. Given at the Canada Room, The Waldorf Astoria, New York. (Hoffer and Osmond's first report on the adrenochrome hypothesis.)

14. Osmond, H & Smythies, J (1952) Schizophrenia: a new approach. Journal of Mental Science. 98(411):309-315, April.

15. Hoffer A, Osmond H & Smythies J (1954) Schizophrenia: a new approach. II. Results of a year's research. J Ment Science 100(418):29-45.