Mental Healthcare Politics and Research

Introduction

There is a big battle going on over universal healthcare. The Republicans claim that this is "socialized medicine". As usual anything designed to help the poor is called "socialism". However, these same Republicans don't call the public schools "socialized schools" or the public libraries "socialized libraries". Public schools give free education to all kids. Public libraries lend books for free to everybody.

All of this does not mean that there will be no problems with universal healthcare. The drug companies may not like it because they may no longer be able to gauge people with absurdly high prices. Some doctors may not like it because they may not be able to charge as much. However, there are very serious problems with our current system. Hospitals have been closing. Nursing homes have been going out of business.

Elderly people can't afford dental care. The poor can't afford dental care. Medicare doesn't cover it.

Mental Healthcare

There are disastrous problems in mental healthcare. Many people are homeless, often with substance abuse. Many people who probably should be in state hospitals are on the streets. But what are the answers? Do they cost more money, or less? The answer may be less. Orthomolecular treatment is cheaper, safer, and more logical than xenobiotic treatment (drugs).

Drugs

"Similarly, it is unclear whether the neuropathological features relate primarily to the therapeutic action of antipsychotics or, more likely, to their predisposition to cause tardive dyskinesia and other motor side-effects."

Harrison PJ.

University Department of Psychiatry, Warneford Hospital, Oxford, UK. paul.harrison@psych.ox.ac.uk

The quote is from Ref. 1. It seems that these drugs cause neuropathology. This has been shown in studies with rats. This makes neuropathology studies of patients more difficult. One way to get around this is to look at old neuropathology studies of patients before the drugs were invented. Harrison himself, an Oxford scientist, did a little of this in Ref. 2. However, most of the studies he reviewed in Ref. 2 were done after the advent of psychiatric drugs. Neuroleptic drugs came out in 1952. The first one was Thorazine.

One such study is Ref. 3 where Southard, a Harvard scientist, reported "lesions and anomalies" in "dementia praecox", which is what schizophrenia was called at the time. These abnormalities were in the cortex. Southard found gliosis, fat deposits, etc.

"Aside from the left-sidedness of the lesions and internal hydrocephalus, very striking is the preference of these changes to occupy the association centres of Fleschig." Southard (3)

Research

Refs. 4 & 5 describe some of the research that has been going on.

"Stevens (1982), in keeping with observations going back as far as Alzheimer (Nieto and Escobar, 1972; Fisman, 1975), found fibrillary gliosis (reactive astrocytosis) in ~70% of her cases of schizophrenia. The gliosis was usually located in periventricular and subependymal regions of the diencephalon or in adjacent basal forebrain structures. As gliosis is a sign of past inflammation (Kreutzberg et al., 1997), this finding supported a number of aetiopathogenic scenarios for schizophrenia involving infective, ischaemic, autoimmune or neurodegenerative processes." Harrison (2)

The main theory is that schizophrenia is a neurodegenerative disease. There was a developmental theory, but it has been repeatedly proven wrong by longitudinal studies that show progressive brain tissue loss in schizophrenia.

Averback (1981)

In 1981 Dr. Paul Averback published two brilliant articles on the neuropathology of schizophrenia. The second one confirmed and extended the first one (7). The second one reported additional lesions that were similar in the nearby septal area of the brain.

"The nucleus of the ansa peduncularis in the substantia innominata frequently contains degenerating neurons in patients with Huntington's disease, Alzheimer's disease, schizophrenia, and possibly other neurological and neuropsychiatric conditions."

Paul Averback, MD (7)

"The cells show massive distention with solvent-extractable lipid-pigment vacuolar droplet material that imparts a distinctive light and electron microscopic appearance." Averback (7)

The septal area had been previously suspected by Dr. R. G. Heath of New Orleans due to abnormal depth EEG readings from that area. Thus Averback's work confirmed Heath.

Averback reported that the Nissl bodies were "barely recognizable". This gives us a very important clue, although Averback himself didn't make much of it. The Nissl bodies store amino acids for the manufacture of proteins. If one or more amino acids were flooding the cells, much of Averback's findings would be explained. Excessive amino acids could destroy the Nissl bodies. Some could be converted to fat, which would explain the fat vacuoles. They could increase the cell's metabolic rate, which would explain the lipofuscin. Amino acids flooding the cells could cause the cells to bloat and to even burst.

A Website for the Layman

Much of the information that I present is on an academic level. However, there is a very good website on mental health which provides information for the layman. THis website is called "HealthyPlace", and it has a URL of www.healthyplace.com.

Conclusions

But what is the treatment, or what are the treatments? My recommendation is orthomolecular treatments. If your brain is allergic to certain amino acids, and since amino acids are found in the diet, wouldn't it make sense to avoid the substances that you are allergic too? However, it may be more complicated than this. Sugar has the effect of pumping more tryptophan into the brain. Tryptophan is an amino acid. Therefore sugar needs to be restricted.

Refs. 11-13, which are available free full text on the Internet, explain more about orthomolecular psychiatry.

References

1. The neuropathological effects of antipsychotic drugs.

Harrison PJ.

Schizophr Res. 1999 Nov 30;40(2):87-99. Review.

2. The neuropathology of schizophrenia. A critical review of the data and their interpretation.

Harrison PJ.

Brain. 1999 Apr;122 ( Pt 4):593-624. Review.

3. Southard EE. On the topographical distribution of cortex lesions and anomalies in dementia praecox, with some account of their functional significance. Am J Insan 1915; 71: 603-71.

4. Roy, P. D., Zipursky, R. B., Saint-Cyr, J. A., et al (1998) Temporal horn enlargement is present in schizophrenia and bipolar disorder. Biological Psychiatry, 44, 418 -422.

5. Schildkraut, J. J. (1965) The catecholamine hypothesis of affective disorders: a review of supporting evidence. American Journal of Psychiatry, 122, 509 -522.

6. Stevens JR. Neuropathology of schizophrenia. Arch Gen Psychiatry 1982; 39: 1131-9.

7. Averback P. Lesions of the nucleus ansae peduncularis in neuropsychiatric disease. Arch Neurol 1981; 38: 230-5.

8. Mettler FA: Anatomy of the basal ganglia, in Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology. Amsterdam, North Holland Publishing Co, 1968, pp 1-55.

9. Mettler FA: Neuroanatomy. St Louis, CV Mosby Co, 1948, pp 355-384.

10. Wolman M: Pigments in Pathology. New York, Academic Press Inc, 1969.

11. www.associatedcontent.com/article/2034097/the_latest_research_in_psychiatry.html
12. www.associatedcontent.com/article/2029268/abnormal_aromatic_metabolism_in_mental.html
13. www.associatedcontent.com/article/2021274/excessive_catabolism_of_tryptophan.html