Â Ref. 1 reported abnormal proteins in schizophrenia. Ref. 3 also reported cerebrospinal fluid abnormalities, but glucose was found to be abnormal. This is of great importance because glucose is the preferred fuel for the brain. The brain cannot burn fats, unlike the rest of the body. The brain can burn amino acids, but not well. It doesn’t make enough ATP from the amino acids.
Â The finding of Ref. 3 supports orthomolecular theories of similarities between schizophrenia and hypoglycemia. The symptoms are similar.
Â Ref. 4 implicates mitochondrial dysfunction in schizophrenia, which is consistent with the slowed glucose metabolism reported by Holmes et al (3).
Â Since many mental diseases may be localized to the brain, a theory favored by the late Linus Pauling, neuropathology may be more effective than biochemistry studies. Ref. 5 is a review of many neuropathology studies. These studies report positive findings. Myelin pathology has been repeatedly reported. this is very interesting because multiple sclerosis often presents with psychiatric symptoms.
Â Russian scientists (Uranova et al) have reported mitochondrial pathology including decreased numbers of mitochondria.
Neurodevelopmental Theory Proven Wrong
Â The every popular but false neurodevelopmental theory has been proven wrong by Ho et alÂ (12) and other similar longitudinal studies. These studies have shown progressive brain tissue loss in schizophrenia.Â I have included a lot of academic references because have been skeptics of my articles. These skeptics can look up the refeences and verify the facts.
Â Theree have been many reports of positive genetic findings in schizophrenia (17). Ref. 17 is consistent with my own view that schizophrenia and bipolar disorder are very similar.
Â Unfortunately psychiatric drugs have been very problematic (18).Â
The Glutamate Theory
Â This theory is very plausible because glutamate is an abundant neurotransmitter in the brain. Ref. 19 is very useful because it is available free full text at Pubmed Central, a National Library of Medicine (US) database on the Web.
“The elevated GLX, if reflecting elevated glutamate, could result from excess neuronal glutamate release or glial dysfunction in glutamate re-uptake. The decreased MI in participants with schizophrenia suggests decreased glial content or dysfunctional glia, which might result from glutamate-mediated toxicity.” Chang et al (19)
The Orthomolecular Approach
Â “If we doctors threw all our medicines into the sea, it would be that much better for our patients and that much worse for the fishes.”Â Oliver Wendell Holmes, M.D.
Â There is a theory that niacinamide, a vitamin, may help Alzheimer’s disease (20, 21). The orthomolecular approach does not use drugs as a rule because of problems as outlined in Ref. 22. Some orthomolecular theory is explained in Refs. 23-25.
Â My own theories are explained in articles on Associated Content (26-28) and in some short articles on Gather. I accept some orthodox medical work, much like Dr. Andrew Weil. However, I also accept some orthomolecular work. There are are some forms of alternative medicine, such as herbal medicine, that I feel aren’t scientific enough.
Â This is not to say that everyting in orthodox medicine is scientific. Orthodox medicine is money-driven. Sometimes the science is to maximize corporate profits. There is more money in drugs than there is in nutrition. However, nutrition is cheaper and safer.
1. Disease Biomarkers in Cerebrospinal Fluid of Patients with First-Onset Psychosis Jeffrey T.-J Huang, F. Markus Leweke, David Oxley, Lan Wang, Nathan Harris, Dagmar Koethe, Christoph W Gerth, Brit M Nolden, Sonja Gross, Daniela Schreiber, Benjamin Reed, and Sabine BahnPLoS Med. 2006 November; 3(11): e428. Published online 2006 November 7.
2.Â Â Thaker GK, Carpenter WT., Jr Advances in schizophrenia. Nat Med. 2001;7:667-671.
3. Holmes E, Tsang TM, Huang TJ, Leweke FM, Koethe D, et al. Metabolic profiling of CSF: Evidence that early intervention may impact on disease progression and outcome in schizophrenia. PLoS Med. 2006. doi: 10.1371/journal.pmed.0030327.
4. Prabakaran S, Swatton JE, Ryan MM, Huffaker SJ, Huang JT, et al. Mitochondrial dysfunction in schizophrenia: Evidence for compromised brain metabolism and oxidative stress. Mol Psychiatry. 2004;9:684-697. 643.
5. Disturbed Structural Connectivity in Schizophrenia-Primary Factor in Pathology or Epiphenomenon? Andreas Konrad and Georg WintererSchizophr Bull. 2008 January; 34(1): 72-92. Published online 2007 May 7.
6. Foong J, Maier M, Barker GJ, Brocklehurst S, Miller DH, Ron MA. In vivo investigation of white matter pathology in schizophrenia with magnetisation transfer imaging. J Neurol Neurosurg Psychiatry. 2000;68:70-74.
7. Foong J, Symms MR, Barker GJ, Maier M, Miller DH, Ron MA. Investigating regional white matter in schizophrenia using diffusion tensor imaging. Neuroreport. 2002;13:333-336.
8. Uranova NA, Casanova MF, DeVaughn NM, Orlovskaya DD, Denisov DV. Ultrastructural pathology of neuronal connectivity in postmortem brains of schizophrenic patients. Schizophr Res. 1996;22:81-83.
9. Uranova NA, Orlovskaya DD, Vikhreva O, et al. Electron microscopy of oligodendroglia in severe mental illness. Brain Res Bull. 2001;55:597-610.
10. Tkachev D, Mimmack ML, Ryan MM, et al. Oligodendrocyte dysfunction in schizophrenia and bipolar disorder. Lancet. 2003;362:798-805.
11. Sigmundsson T, Suckling J, Maier M, et al. Structural abnormalities in frontal, temporal, and limbic regions and interconnecting white matter tracts in schizophrenic patients with prominent negative symptoms. Am J Psychiatry. 2001;158:234-243.
12. Ho BC, Andreasen NC, Nopoulos P, Arndt S, Magnotta V, Flaum M. Progressive structural brain abnormalities and their relationship to clinical outcome: a longitudinal magnetic resonance imaging study early in schizophrenia. Arch Gen Psychiatry. 2003;60:585-594.
13. Buchsbaum MS, Tang CY, Peled S, et al. MRI white matter diffusion anisotropy and PET metabolic rate in schizophrenia. Neuroreport. 1998;9:425-430.
14. Smesny S, Rosburg T, Nenadic I, et al. Metabolic mapping using 2D (31)P-MR spectroscopy reveals frontal and thalamic metabolic abnormalities in schizophrenia. Neuroimage. 2007;35:729-737.
15. Uranova NA, Vostrikow VM, Orlovskaya DD, Rachmanova VI. Oligodendroglial density in the prefrontal cortex in schizophrenia and mood disorders: a study from the Stanley Neuropathology Consortium. Schizophr Res. 2004;67:269-275.
16. Black JE, Kodish IM, Grossman AW, et al. Pathology of layer V pyramidal neurons in the prefrontal cortex of patients with schizophrenia. Am J Psychiatry. 2004;161:742-744.
17. Berrettini W. Evidence for shared susceptibility in bipolar disorder and schizophrenia. Am J Med Genet. 2003;123:59-64.
18. Goodwin FK, Bunney WE Jr. Depressions following reserpine: a reevaluation. Semin Psychiatry 1971;3:435-48.
19. Brain metabolite abnormalities in the white matter of elderly schizophrenic subjects: implication for glial dysfunction Linda Chang, Joseph Friedman, Thomas Ernst, Kai Zhong, Nicholas D. Tsopelas, and Kenneth DavisBiol Psychiatry. Author manuscript; available in PMC 2008 December 15. PMCID: PMC2222890 Published in final edited form as: Biol Psychiatry. 2007 December 15; 62(12): 1396-1404. Published online 2007 August 13. doi: 10.1016/j.biopsych.2007.05.025.
20. Vitamin Holds Promise for Alzheimer’s Disease. Randy Dotinga, HealthDay Reporter, Nov 5, 2008.
21. Green KN, Steffan JS, Martinez-Coria H, Sun X, Schreiber SS, Thompson LM, LaFerla FM. Nicotinamide restores cognition in Alzheimer’s disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotau. J Neurosci. 2008 Nov 5;28(45):11500-10.
22. Classen DC, Pestotnik SL, Evans RS, Lloyd JF, Burke JP. Adverse drug events in hospitalized patients. Excess length of stay, extra costs, and attributable mortality. JAMA. 1997 Jan 22-29;277(4):301-6.
23. Hoffer A and Foster HD. Feel Better, Live Longer With Vitamin B-3: Nutrient Deficiency and Dependency. CCNM Press, 2007. ISBN-10: 1897025246; ISBN-13: 978-1897025246.
24. Foster HD. What Really Causes Alzheimer’s Disease. Trafford, 2004. ISBN 1-4120-4921-0.
25. Hoffer A. Mechanism of action of nicotinic acid and nicotinamide in the treatment of schizophrenia. In: Hawkins D and Pauling L: Orthomolecular Psychiatry: Treatment of Schizophrenia. San Francisco: W.H. Freeman. 1973; p. 202-262.