Many diseases are caused by errors in metabolism. These include Alzheimer's disease, Huntington's chorea, schizophrenia, diabetes, mental retardation, etc. Mental retardation is a cluster of different diseases, many of which are different errors in metabolism that are inherited. These matters are often treatable by diet.
In the case of schizophrenia, there is massive evidence for an error in brain glucose metabolism, much like a form of cerebral diabetes. Japanese researchers have reported carbohydrate deposits in the brains of schizophrenics. This suggests that the problem is not due to any lack of glucose, but rather is due to the fact that, for some reason, the brain is burning something else for fuel (such as amino acids).
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The Metabolism in Schizophrenia
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There is a chain of metabolic errors that cause schizophrenia, as there is in PKU (a form of mental retardation with psychiatric symptoms). Error A causes error B, error B causes error C, etc. A toxin is formed in the brain by abnormal methylation of dopamine. This toxin is DMPEA (3,4-dimethoxyphenylethylamine).
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A study reported in the Journal of Neurochemistry in 1996 reported that DMPEA had an adverse effect on "mitochondrial respiration and complex I activity". "Compunds with dimethoxy residues in the phenyl ring were associated with more potent inhibition of complex I than those without." DMPEA has two such dimethoxy groups. The authors report DMPEA as a mitochondrial toxin. They theorized that it might be involved in Parkinson's disease.
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DMPEA a Neurotoxin
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There have been many reports in the literature on DMPEA. All recent reports show it to be toxic. A Florida report (Charlton & Crowell, 2000) involved a study in which the substance was tested on rats. It was found to be "behaviorally active".
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Dopamine has more than one route of metabolism. In one route it is converted to norepinephrine, which is then converted to epinephrine by methylation. Another route is methylation of dopamine involving the hydroxyl groups on the benzene ring.
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CARBOHYDRATE DEPOSITS IN THE BRAINS OF PATIENTS WITH SCHIZOPHRENIA
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In the year 2000 a Japanese group, Nishimura et al, reported carbohydrate deposits in the brains of patients with schizophrenia, Down's syndrome, and dementia. They suggested "unusual glycometabolism in neurons may disturb the neuronal function and cause brain disorders. The deposits were spherical.
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ALZHEIMER'S DISEASE
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The hippocampus is involved with recognition and memory. Pathology has been reported in this area in "Alzheimer type dementia". The Japanese group mentioned above studied 6 cases of Alzheimer's disease and used 22 cases of normal controls. The controls were "without brain disorders". Carbohydrate deposits were found. The spherical deposits had "an extracellular matrix origin". "Neuronal degeneration" was reported.
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CHINESE MEDICINE
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There are over a billion people in China. These people have done a lot of work. It would seem to be an error to overlook the work of these people, but Chinese medicine has been largely ignored in the US, except by those favoring alternative medicine. What is considered alternative medicine in the US is similar to orthodox medicine in China, where plants are considered to have healing powers. One such medicine is a fermented tea which comes from a Manchurian plant (a lichten). This tea is considered to have healing powers. It is not the same as green tea, which comes from leaves of a different plant. However, green tea is also thought to have health benefits. These benefits are thought to come from the polyphenol components.
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KOMBUCHA TEA
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This tea is considered a panacea by some people. One theory is that it detoxifies the body. How it does this is controversial. There is a substance called glucuronic acid which binds to toxins. The glucuronic acid can be made from glucose. According to this theory, bacteria make the glucuronic acid. Whether glucuronic acid is present in Kombucha tea is controversial. This is a plausible theory because DMPEA is conjugated as a glucuronide. DMPEA also conjugates with sulphate.
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PARTICLES IN THE CEREBROSPINAL FLUID IN SCHIZOPHRENIA
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In 2002 a Swedish group, Wetterberg et al, reported "micrometer-sized particles in cerebrospinal fluid (CSF) in patients with schizophrenia". These particles were found in 20 of the 22 patinets with schizophrenia, but in only 2 of 38 controls (P<0.001). Analysis "did not reveal bacterial DNA material in the particles". "The particles have not replicated in culture." This signifies that the particles are not microorganisms. The authors thought they were "biological disease markers in schizophrenia". They did not know whether the particles caused the disease or resulted from the disease.
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Fetal Research
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I have often wondered why Diana Orlovskaya, the brilliant female Russian neuropathologist, never won the Nobel Prize in Medicine. However, she still has a chance as she is still doing reserch. Perhaps the reason she did not get the prize is she did research on aborted fetuses in 1975. She studied "ultrastructural features of brain cells from the embryos of schizophrenic women."
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Orlovskaya et al (1975)
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This Russian group used the electron microscope to study embryonic brain tissue. There were "ultrastructural peculiarities of the cell elements". There were "damages of membranes, mitochondrias, and accumulated material in the cytoplasm". The mitochondria provide energy for the cell. Damage to the mitochondria can cause an error in energy metabolism. Damage to the cell membrane can cause problems in transport, including a possible loosening of the blood-brain barrier.
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Yun et al (1992)
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In 1992 Yun et al published an artical on human cerebrospinal fluid proteins. "Proteins that are not present on the normal map, but appear in spinal fluid in patients with schizophrenia and Creutzfeldt-Jacob disease are illustrated on additional maps. Electrophoresis (two-dimensional) was used. These scientists were from the California Institute of Technology (Cal Tech) in Pasadena. This was the college where Linus Pauling first taught before moving to Stanford. Pauling's controversial views may have been a source of friction. Nevertheless, Pauling wrote a brilliant chemistry textbook while at Cal Tech.
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Abnormal Cerebrospinal Fluid Proteins
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A similar report was published in Paris in 1972 by Sizaret et al. They reported "abnormal cerebrospinal fluid proteins in schizophrenia". At first glance these reports appear to contradict the DMPEA theory because DMPEA is a small molecule. However, DMPEA binds to a globulin, according to Bergen of Massachusetts. Sizaret et al reported that the offending proteins were beta-globulins. Paranoid schizophrenics were studied. The globulins are in the serum, which is part of the blood. However, the French group studied the cerebrospinal fluid.
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Soloveva et al (1970)
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In 1970 Soloveva et al found a toxic serum factor in the blood of schizophenics using a cat ganglion (nerve) as an assay. Mitochondrial swelling was seen. The endoplasmic reticulum was abnormal.
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Vilkov et al (1986)
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Even more evidence for an unknown toxic factor comes from another Russian group, Vilkov et al. This group reported "biochemical and ultrastructural changes in animal brain after intracisternal administration of the cerebrospinal fluid from patients with schizophrenia". Rabbits and rats were used in the assay. The "liquor" was "cytotoxic". They suggested "antibrain" substances.
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Neuropathology Reflects Metabolic Errors
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The Vogt family, including Cecile & Oskar Vogt of Germany and Marthe Vogt of Edinburgh, Scotland, used neuropathology to try to ferret out the metabolic errors that cause disease. In 1951 C. Vogt & O. Vogt reported a study of Huntington's chorea and schizophrenia. Huntington's chorea is hereditary. They reported pathology in the striatum in schizophrenia. Most of the cells were damaged. They were wasting cells, or "schwundzellen". Their cytoplasm became progressively vacuolated and then disappeared whereas "their nucleus remained relatively unaltered".
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Heath's Neurophysiological Approach
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Heath used both biochemical methods and neurophysiological methods. He studied the septal area of the brain because he found abnormal electrical effects in this area in schizophrenics. The patients showed classical psychotic symptoms when the recording abnormalities appeared on the depth EEG. He implanted electrodes in the brain. Septal spiking was seen. This technique was used as an assay for a serologic fraction extracted from the blood of schizophrenics, which he named "taraxein". The fraction was injected into monkeys, which then showed severe behavioral symptoms. At first Heath thought the fraction was similar to ceruloplasmin, an alpha-2-globulin. Further study showed it to be a different globulin. This work was confirmed by Hoagland et al, who thought that there was a tightly bound small molecule attached to the globulin.
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Lozovskii et al (1977)
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This Russian group reported increased serum lactate dehydrogenase activity in schizophrenia. They reported that this effect was due to "additive polygenic inheritance with threshold manifestation". Twins were studied. Some of the twins were dizygotic and some of the twins were monozygotic (identical). There was a correlation between enzyme activity in schizophrenics and in their relatives. This correlation was "marked".
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Mukhin & Faktor (1979)
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This work continued the previous Russian work and may explain why the enzyme was high. Muhkin & Faktor reported a "stimulating effect of schizophrenic patients' plasma on the cellular incorporation of tryptophan". Hemolysis was seen perhaps due to flooding of the erythrocytes with tryptophan, which is an amino acid. Hemoglobin was released from the erythrocytes, suggesting that the cell membranes were ruptured. The cytoplasmic enzyme lactate dehydrogenase was increased. This suggests that the tryptophan was converted into alanine and then into pyruvate, which in turn can be converted into lactate. Thus at least one amino acid is flooding the glycolytic pathway.
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Phenylketonuria
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This disease is an inborn error of metabolism which results in mental retardation. In 1998 Shiwach & Sheikha reported "delusional disorder in a boy with phenylketonuria ..." "He did not respond to a traditional antipsychotic medication ..." The authors considered him "dually diagnosed". They felt that this case supported "the prevalent biogenic amine theories in psychiatric disorders". However, this author (Olson) feels that the case supports the amino acid flooding theory of schizophrenia. According to this theory, amino acids flood the brain cells in schizophrenia causing a disruption of carbohydrate metabolism. In other words, amino acids are burned for fuel by the brain instead of glucose with disastrous results. In this case the amino acid flooding the brain is phenylalanine.
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