The Riddle of Mental Illness

Several reports have appeared in the professional literature implicating mitochondrial dysfunction as causing schizophrenia. In March 2001 a report appeared in Schizophrenia Research by Maurer et al of Germany. This paper reported "evidence for a mitochondrial oxidative defect in brains of patients with schizophrenia".

Maurer et al (2001)

This report claims "an impairment of energy metabolism in brains of patients with schizophrenia". "Decreased oxidative metabolism has been consistently documented in the frontal lobes." Measurements by the German group "confirm a defect of oxidative phosphorylation in brains from patients with schizophrenia, which may contribute to impaired energy generation". Post-mortem brain specimens were used. The maximum reductions were in the frontal cortex, the temporal cortex, and the basal ganglia. There was no reduction in the cerebellum.

Ben-Shachar (2002)

This report came from Israel. Ben-Shachar recommended ""novel treatment approaches". The author suspected "linkage to dopamine". The author claimed "altered cerebral energy metabolism".

Uranova and Aganova (1989)

This report related the results of microscopic analysis of autopsy specimens. They reported deformation and reduction in the number of mitochondria. Similar results were reported by Kung and Roberts (1999). Kolomeet and Uranova (1999) reported similar findings.

Prabakaran et al (2004)

This report appeared in Molecular Psychiatry. The University of Cambridge group in England reported "mitochondrial dysfunction in schizophrenia". They used techniques called transcriptomics, proteomics, and metabolomics. They reported "confounding drug effects could be ruled out". "Altered proteins" were reported by the British group. They suggested "compromised brain metabolism". This is certainly food for thought. What to do in the way of treatment is not yet clear, unfortunately. My own opinion is that a diet might help.

Averback (1981)

In 1980 Dr. Paul Averback was with the prestigious University of Cambridge in England. Dr. Averback studied an obscure area in the basal ganglia called the "nucleus ansae peduncularis". The NAP is a group of large ganglionic cells "in the vicinity of the substantia innominata" according to Averback (1981). Averback reported "lipid-pigmentary neuronal degeneration" in this area in schizophrenia. This appears to confirm earlier (1913) work by Alzheimer. Averback used the neuroanatomy system of Mettler. Mettler divided the substantia innominata into 7 regions, including the NAP as one of these regions. Averback reported "remnants of degenerate cells that appear to have been extremely distended." He reported that his findings were not the same as those found in neuronal ceroid lipofuscinosis.

The "bulbous distortion" of neurons reported by Averback could be caused by these cells overeating some macronutrients such as amino acids. Since the basal ganglia are very high in dopamine, the possibility exists of an error in dopamine metabolism. Averback reported that his findings were not the same as the "granulovacuolar degeneration" found in Alzheimer's disease. He found "masses of lipid vacuoles". Autoflourescence was seen. This was due to a pigment material. The stored material appeared similar to lipofuscin.

Carbohydrate Deposits

There are people who will not like this article because it does not fit in with their preconceived notions. I have pruned some of these people from my mailing list, but not all. The reason is that I would like to enlighten the powers that be regarding these issues as the issues are tremendously important. A brilliant Japanese group of scientists has reported carbohydrate deposits in the brains of schizophrenics. This very recent report confirms years of evidence suggesting defective glucose metabolism in the brains of schizophrenics.

Neuropathology Results

Using the electron microscope, a brilliant group of scientists from Moscow studied the brains of people with "severe mental illness". This work was reported July 2001 in Brain Research Bulletin. Uranova et al studied the oligodendroglia and myelinated neurons. Glial cells support and nourish neurons. Damage to the myelin sheaths was reported. The prefrontal area and the caudate nucleus were studied. Both areas are high in dopamine. Pathology of the oligodendroglia was reported in both schizophrenia and "bipolar disorder". "Bodies" were reported in the neurons. Analysis "demonstrated that these changes could not be explained by artifacts of postmortem delay, age, neuroleptic medication, or gender". "Apoptosis" and "necrosis" were found. "Necrosis" means cell death. The mitochondria were abnormal, suggesting an error in energy metabolism.
Conclusions

It can be concluded that much of the theory of antipsychiatry is a mockery of a travesty. Notions that there is no organic basis for schizophrenia are false. The results support both orthodox psychiatry and orthomolecular psychiatry. The fact that similar pathology is seen in both schizophrenia and bipolar disorder calls into question the classification of mental diseases, which dates back to Kraepelin.

Craig Olson, Brighton, MA