Taraxein: The Cause of Schizophrenia?

"It has been suggested by B. Melander and S. Martens, Dis. Nerv. Syst. 19, 478 (1959); Acta Psychiat. Neurol. Scand. 34, 344 (1959). and by A. Hoffer and H. Osmond, Int. J. Neuropsychiat. 2, 1 (1966), that the effects of taraxein. [R. G. Heath. S. Martens, B. E. Leach, M. Cohen, C. A- Feigley, Amer. J. Psychiat. 114, 917 (1958)] may result from changing the permeability of the blood-brain barrier." Pauling (1968)

"You already have the precious mixture that will make you well. Use it." - Rumi

Introduction

"The concentration of trytophan, quinolinic acid, kynurenic acid, serotonin and 5-hydroxyindoleacetic acid was found to be higher in the plasma of patients with all these disorders ..." Ravikumar A, Deepadevi KV, Arun P, Manojkumar V, Kurup PA
Department of Neurology, Medical College, Trivandrum, and Metabolic Disorders Research Centre, Puliyarakonam, Trivandrum, India.

This quote is from Ref. 1. The fact that serotonin was found to be high is in direct contradiction to the serotonin deficiency theory favored by drug companies that make SSRI drugs. These SSRI drugs raise serotonin.

But what causes the hypercatabolism of tryptophan? The answer may be "taraxein", a protein found only in schizophrenics. Taraxein has been very controversial. Positive findings have been reported in the US, Sweden, the USSR, Canada, etc. A toxic factor in the blood was also reported in Norway, but the Norway researchers did not call it "taraxein". The same is true of researchers from Israel.

The catabolism of tyrosine was also reported to be abnormal (2).

Tryptophan

"Alteration in tryptophan catabolism has been reported in neurodegenerative disorders like Huntington's disease." Ravikumar A, et al (2000)

Ref. 3 provides more information on tryptophan.

The abnormality in tyrosine metabolism reported in Ref. 1 could reflect the production of taraxein, which could be made from tyrosine. Taraxein could cause tryptophan to flood the cells, which would explain the elevation of serotonin and other tryptophan metabolites seen.

More Research Needed

There should be more funding for all types of medical research. The drug companies fund some projects, but these don't get published unless they come out the way the drug company wants them to. Unfortunately there are a lot of problems with psychiatric drugs (4). Unfortunately atypical "antipsychotics" can cause abnormal glucose metabolism (5).

Bipolar Disorder

Abnormal tryptophan metabolism has been also reported in bipolar disorder (6). Ref. 7 reports similarities between bipolar disorder and schizophrenia. They could be two different points on a continuum. There is also a dopamine theory for bipolar disorder (8). Both theories could be true. An error in dopamine metabolism, presumably "taraxein", could cause the excessive tryptophan metabolism.

Schizophrenia

Ref. 9 reports excessive tryptophan metabolism in schizophrenia in the nervous system. Ref. 10 reports glycolysis dysfunction in schizophrenia. Such glycolysis dysfunction could be caused by excessive tryptophan entering the brain. The brain might burn tryptophan for fuel instead of glucose in an effort to reduce the tryptophan excess. Ref. 11 is by the same German group that wrote Ref. 10.

Conclusions

The name "taraxein" was invented by Health and his Tulane group in the Fifties. They weren't sure exactly what their substance was, so they called it "taraxein". This name enjoyed a brief popularity, but has largely died out. I am probably the only current writer who uses it.

Health found taraxein to be a large protein with a small molecule attached to it. The small molecule was thought to be the active substance, and the protein was a carrier molecule. Heath is now deceased, unfortunately.

References

1. Tryptophan and tyrosine catabolic pattern in neuropsychiatric disorders. Ravikumar A, Deepadevi KV, Arun P, Manojkumar V, Kurup PA. Neurol India. 2000 Sep;48(3):231-8.

2. http://www.neurologyindia.com/text.asp?2000/48/3/231/1530.

3. Andrew Freese BA, Kenton J Swartz et al : Kynurenine metabolites of tryptophan implications for neurological diseases. Neurology 1990; 40 : 691-695.

4. Buchholz S, Morrow AF, Coleman PL. Atypical antipsychotic-induced diabetes mellitus: an update on epidemiology and postulated mechanisms. Internal Medicine Journal. 2008;38(7):602-606.
5. Scheen AJ, De Hert MA. Abnormal glucose metabolism in patients treated with antipsychotics. Diabetes and Metabolism. 2007;33(3):169-175.

6. J Psychiatry Neurosci. 2010 May;35(3):195-9. Elevated levels of kynurenic acid in the cerebrospinal fluid of patients with bipolar disorder. Olsson SK, Samuelsson M, Saetre P, Lindström L, Jönsson EG, Nordin C, Engberg G, Erhardt S, Landén M.

7. Lichtenstein P, Yip BH, Bjork C, et al. Common genetic determinants of schizophrenia and bipolar disorder in Swedish families: a population-based study. Lancet. 2009;373:234-9.

8. Berk M, Dodd S, Kauer-Sant'anna M, et al. Dopamine dysregulation syndrome: implications for a dopamine hypothesis of bipolar disorder. Acta Psychiatr Scand Suppl. 2007;434:41-9.

9. Erhardt S, Blennow K, Nordin C, et al. Kynurenic acid levels are elevated in the cerebrospinal fluid of patients with schizophrenia. Neurosci Lett. 2001;313:96-8.

10. J Psychiatr Res. 2010 May 14. Proteome analysis of the thalamus and cerebrospinal fluid reveals glycolysis dysfunction and potential biomarkers candidates for schizophrenia. Martins-de-Souza D, Maccarrone G, Wobrock T, Zerr I, Gormanns P, Reckow S, Falkai P, Schmitt A, Turck CW.
11. World J Biol Psychiatry. 2010 Mar;11(2):110-20. Proteome analysis of schizophrenia brain tissue. Martins-De-Souza D, Dias-Neto E, Schmitt A, Falkai P, Gormanns P, Maccarrone G, Turck CW, Gattaz WF.