A Brief History of Scientific Psychiatry

The history of psychiatry is so vast that I will most likely write a series of articles on it. There has been a lot of false theories and quackery, but I prefer to concentrate on the valid material. This narrows it down quite a bit. I will leave out the myths of Thomas Szasz and other eccentrics.

A 2004 psychiatric textbook by Yudofsky & Hales reported "a remarkable reduction in glucose metabolism in the medial temporal structures". This is the type of material that I find interesting. Temporal lobe epilepsy often is accompanied by psychiatric symptoms. The term "medial" refers to structures near the midline. This same area has been the site of many positive neuropathology findings.

Neuropathology

Perhaps the first scientific approach used in psychiatry was that of neuropathology. Neuropathologists have examined the brain of mental patients for centuries.

On of the first brilliant articles was that of the German psychiatrist Alois Alzheimer in 1897. Alzheimer reported various abnormalities in "dementia praecox". This work was confirmed by Scioli in 1909. Scioli found an increase in fat, glial proliferation, and ameboid cells. Glial proliferation is seen in toxic diseases. This suggests that mental disease is caused by an unknown toxin.

I interpret the fat to indicate a metabolic disorder. The brain cells may be overeating some macronutrients due to a transport error. Perhaps the toxin causes this problem.

Papez

In 1944 James Papez reported "neuronal disease associated with intracytoplasmic inclusion bodies" in mental patients. In 1949 Papez & Bateman reported "cytological changes in nerve cells in dementia praecox". "Dementia praecox" is an old term for what is now called "schizophrenia".

In 1956 Papez & Papez reported "drops of protein" in "clouded and catatonic states". This appears to suggest an error in protein metabolism. Papez also found amyloid bodies, which are starch deposits. These bodies suggest a possible slowing of glucose metabolism.

Averback (1981)

In 1981 Averback reported "lesions of the nuceus ansae peducularis in neuropsychiatric disease". He found massive bloating & death of neurons in schizophrenia, Alzheimer's disease, and Huntington's chorea. He reported "the Nissl substance may not be recognizable in the extreme examples". Since the Nissl bodies house amino acids, this suggests that amino acids may be the problem. In other words, amino acids are flooding the brain cells.

Gurd

In 1920 Gurd of the US reported "loss of chromatin" and "fatty degeneration". The loss of chromatin is consistent with Averback's report of destruction of the Nissl bodies, which contain chromatin. Chromatin is genetic material such as RNA. There could be a loss of RNA if excessive amino acids are flooding the cells because RNA is used to make proteins from them. Excessive amino acids could also convert to fat.

Conclusions

I have only scratched the surface of the work done in psychiatry. Perhaps my next report on this subject might deal with the history of biochemical work in psychiatry, which is related to the neuropathology.

Unfortunately there have been a lot of problems with drugs due to the toxic side effects. Therefore I recommend a diet very low in amino acids. There are probably people who will balk at this because for most people amino acids are valuable. However, one man's medicine is another man's poison. This is due to biochemical individuality.

References

1. Uranova, N. et al (2001) Electron microscopy of oligodendroglia in severe mental illness. Brain Res. Bull. 55, 597-610.

2. Averback, P. (1981) Lesions of the nucleus ansae peduncularis in neuropsychiatric disease. Archives of Neurology, 38, 230-235.

3. www.associatedcontent.com/article/470898/an_introduction_to_neuropathology.html .

4. www.associatedcontent.com/article/463405/brilliant_russian_research_on_schizophrenia.html
5. www.associatedcontent.com/article/456611/the_healing_substances_found_in_plants.html
6. www.associatedcontent.com/article/458187/abnormal_tryptophan_metabolism_in_depression