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What causes Schizophrenia?


Michaelangelica

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About 1 percent of the world's population -- including 2.4 million Americans -- has schizophrenia, a complex and puzzling mental illness that can lead to delusions, hallucinations and disordered thinking. It is one of the world's most common causes of psychosis, according to Bahn. Since it was first described more than 100 years ago, scientists have made little progress in unraveling the causes of the disease, and no definitive test is available to diagnosis it, she says.

 

"We desperately need a better understanding of this illness. It is, however, difficult to study the disease, as the brain can't easily be investigated. We can't take multiple biopsies from patients to look at the disease-related changes," Bahn says. "We need a new concept."

Abnormal Proteins Linked To Schizophrenia Found In Body Tissue
Toxoplasma gondii and Schizophrenia

Posted 12/03/2003

E. Fuller Torrey, Robert H. Yolken

Abstract and Introduction

Abstract

 

Recent epidemiologic studies indicate that infectious agents may contribute to some cases of schizophrenia. In animals, infection with Toxoplasma gondii can alter behavior and neurotransmitter function. In humans, acute infection with T. gondii can produce psychotic symptoms similar to those displayed by persons with schizophrenia.

Log In Problems

 

White said toxoplasmosis also may be linked to some cases of schizophrenia and bipolar disease.
Cluster Of Journals Publish MSU Findings On Common Parasite

 

"SCHIZOPHRENIA is a cruel disease," Torrey has written, with considerable understatement. Although it affects only 1 percent of the population, schizophrenia is among the most debilitating forms of mental illness.

. . .

For Torrey, Ewald, and others, that means looking for some kind of infectious agent that may exploit a genetic weakness when invading a host. This interplay of genetics and infectious disease is complex

. . .

Of the other diseases that Yolken tried to correlate with schizophrenia -- rubella, influenza, cytomegalovirus, chlamydia, and herpes simplex 2 (HSV-2) -- only herpes was significant.

Tests showed that mothers of schizophrenic children were 5.8 times more likely to have antibodies to HSV-2 than mothers of the healthy controls.

 

How might a herpes infection contracted in the womb lead to mental illness years later?

As Yolken sees it, the age when most schizophrenics first develop symptoms suggests exposure to some sort of "infectious agent which has a higher rate of transmission in late adolescence and early adulthood."

 

Yolken hypothesizes that the herpes virus remains quiescent in the brain until adolescence, when it is triggered by the Epstein-Barr virus that causes mononucleosis, also known as the kissing disease.

 

Another theory holds that it is reactivated by another version of itself picked up in sexual contact.

How such an infection translates into schizophrenia is still a matter of considerable speculation.

. . . ALTHOUGH Torrey and Yolken's theory that an infectious disease causes schizophrenia has gained some acceptance, or at least respect, it is still far from the prevailing view.

Torrey in particular has many critics, even among colleagues with whom he has collaborated. Take Irving Gottesman, a professor of psychology and clinical pediatrics at the University of Virginia and a major proponent of genetic explanations of schizophrenia.

The two men maintain a friendly relationship despite their differences. "The thing that keeps us together," explains Gottesman, "is that we have common enemies: the Freudians, the sociologists, the cultural anthropologists" -- anyone, in other words, who wants to ascribe schizophrenia to nonbiological causes.

They frequently co-author articles attacking what they perceive to be misallocations of mental health research funds. But when it comes to explaining schizophrenia, they part ways.

. . .

"Viruses could be epigenetic contributors, too,"

. . .

Neurodevelopmental thinking nonetheless remains at the center of current psychiatric accounts of schizophrenia. And though Torrey and Yolken's views currently sit on the margins, Ewald does not think they will remain there. "Infectious causation has been seriously underestimated from the 1800s onward," he notes. "Many people who suggested infectious causes of diseases were dismissed but later proven right." Take gastric ulcers

. . .

Torrey on schizoviruses (interview)

 

Abstract

 

Winter birth, urban birth and/or childhood residence, and perinatal complications have each been identified as environmental risk factors for the later development of schizophrenia, schizoaffective disorder, and bipolar disorder. A preliminary case–control study also identified cat exposure in childhood as a possible risk factor

.ScienceDirect - Schizophrenia Research : The antecedents of psychoses: a case–control study of selected risk factors

 

Abnormalities in glutamate receptors.

Glutamate, an amino acid known to affect dopamine and excite nerve activity, is also under scrutiny. For example, glutamate binds to N-methyl-D-aspartate (NMDA) receptors, which play a critical role in healthy nerve development and may be abnormal in schizophrenia. Abnormalities in NMDA and other molecules in the glutamate pathway appear to play significant roles in impairment of mental function and development of negative symptoms. Calcineurin, a protein that regulates the NMDA receptor, plays a role in cognition and is now recognized as a marker of risk for schizophrenia

Schizophrenia

Articles

The Role of Infections in Mental Illness

 

by Frank Strick, Clinical Research Director

THE RESEARCH INSTITUTE FOR INFECTIOUS MENTAL ILLNESS (RIIMI)

Call 1800 6992466 then press pound (#) 8314255555

E-mail: [email protected]

San Francisco, USA

Other Notes: They serve clients world-wide via phone consultations.

 

In considering an infectious etiology to any chronic mental illness there are at least four categories to consider.

First are those infections already recognized to induce psychiatric symptoms. These include pneumonia, urinary tract infection, sepsis, malaria, Legionnaire's disease, syphilis, typhoid, diphtheria, HIV, rheumatic fever and herpes. (Ref: Chuang)

 

While the psychiatric effects of these infections are known to the medical field, they are rarely screened for if the initial presentation is made to a mental health professional.

Moreover, the significance of some of these infections may date back to prenatal development.

Research done at the John Hopkins Children's Center and published in the Archives of General Psychiatry in 2001 found that mothers with evidence of Herpes Simplex Type 2 infection at the time of pregnancy had children almost six times more likely to later develop schizophrenia.

And in the US, Europe and Japan, birth clusters of individuals who develop schizophrenia later in life closely mirror the seasonal distribution of Ixodes ticks at the time of conception (Lyme disease).

 

Second are those parasitic infections such as neurocysticercosis where the brain is directly invaded by the infective agent through a well-established, imageable (visible on brain scan) mechanism (cysts, lesions, cerebral swelling etc.) Signs of psychiatric disease (depression and psychosis) were found in over 65% of neurocysticercosis cases (caused by a tapeworm whose incidence in the US is rising due to demographic increases in foreign immigrant populations.) [Ref: Forlenza]

While the mechanisms for psychiatric manifestations are easy to demonstrate when brain tissue is directly affected, there are also multiple documented reports in the literature of psychiatric symptoms associated with other parasites like giardiasis, ascaris (roundworm), trichinae (cause of trichinosis), and Lyme borrelia and viruses like borna virus.

Documentation also exists of these psychiatric symptoms resolving when the underlying hidden infection is treated.

 

Dr. J. Packman of Yale University wrote over ten years ago that "Patients with parasitic loads are more likely to exhibit mental status changes and there is an improvement in mental status of a subset of psychiatric patients following treatment for parasites."

In fact, a review of 1300 human cases of trichinosis in Germany found CNS (central nervous system) involvement in up to 24% of the cases (Menningeal inflamation or encephalitis). [Ref: Froscher]

 

Clinically, in cases like neurocysticercosis, the problem is not the lack of a well-defined mechanism but the lack of mental health practitioners qualified to make such a diagnosis or even suspect it.

Even infectious disease specialists tend to underestimate the scope of the problem, in part due to underreporting (neurocysticercosis is not a reportable condition in most states and the incidence of trichinosis is, we believe, vastly underestimated according to newly developed antibody assays only made available in 2003)

. . .

Next are those parasitic, bacterial and viral infections like toxoplasmosis and strep where a strong statistical link to mental illness has been demonstrated but research is underway to establish a causal connection. In humans acute infection with toxoplasmosis gondii can cause brain lesions, changes in personality and symptoms of psychosis including delusions and auditory hallucinations..

The Role of Infections in Mental Illness

 

 

Evidence is mounting to link toxoplasmosis with schizophrenia

Disease/Infection News

Published: Tuesday, 18-Oct-2005

 

Keep pet cats inside, stop feeding strays, cook meat sufficiently and reconsider the way the veterinary profession and public health agencies think - and teach - about the zoonotic pathogen Toxoplasma gondii.

Such are the recommendations of Milton M. McAllister, a professor of pathobiology in the College of Veterinary Medicine at the University of Illinois at Urbana-Champaign.

 

He delivered that message in Christchurch, New Zealand, at the 20th International Conference of the World Association for the Advancement of Veterinary Parasitology.

 

McAllister, also a clinical professor of pathology in the U. of I. College of Medicine at Urbana-Champaign, made his case based on his review of numerous studies on the animal-carried pathogen during the past decade.

His review, prepared for the conference, appeared in the Sept. 30 issue of the journal Veterinary Parasitology.

 

"Our profession needs to come to grip with the accumulating body of evidence about the tremendous burden wrought on society by toxoplasmosis," McAllister wrote. "Further research is needed to clarify the association between toxoplasmosis and mental health, but until such time that this association may be refuted, it is my opinion that the current evidence is strong enough to warrant an assumption of validity."

Evidence is mounting to link toxoplasmosis with schizophrenia
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Good articles, Michaelangelica, and I think there might be good reason to suspect that viruses or bacteria could be among the causes. IIRC, herpes viruses (HSV-1 and -2) can infect neurons and can become latent, which may provide some basis for the explanation that they could cause schizophrenia or other mental disease, through altering or damaging the neurons of the brain. Another example would be HIV and AIDS. If HIV invades the brain and become established in neurons, late in AIDS, it may be manifested through psychosis or other mental disease. In most people, herpes viruses do invade some neurons, but are kept under control by the immune system.

 

WHO | Sexually Transmitted Diseases

 

Babies are particularly at risk for infection and serious complications from herpes viruses, because their immune systems are not well developed and can't control the viruses quickly enough. Babies can become blind or brain-damaged if they get herpes infections.

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In most people, herpes viruses do invade some neurons, but are kept under control by the immune system.

 

WHO | Sexually Transmitted Diseases

 

Babies are particularly at risk . . Babies can become blind or brain-damaged if they get herpes infections.

Thanks,

On STD's This is a hoot

The 12 STIs Of Christmas

 

Your WHO link is shocking. I couldn't believe this:

Genital herpes is one of the most common ulcerating diseases of the genital mucosa. It is estimated that in the USA, for example, from 40 to 60 million people are HSV-2-infected, with an incidence of 1–2 million infections and 600 000–800 000 clinical cases per year. Prevalence in the 30–40 year-old population is about 30%.

. . .

There is now ample evidence that HSV-2 infection is a major cofactor of HIV infection

and

. . .

Various studies have estimated that there are four to five million new cases of chlamydial infection each year in the USA alone. Among urban adolescent females, the incidence rate can be as high as 30%. The annual costs of treating and caring for patients with PID might be as high as US$10 billion.

 

We know syphilis causes brain problems. Do you know much about the others?

 

 

Would't it be remarkable if this terrible disese,Schizophrenia, scourge of mankind for eons , could be cured by an anti-viral pill.

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  • 2 weeks later...
Good articles, Michaelangelica, and I think there might be good reason to suspect that viruses or bacteria could be among the causes..

Thanks maikeru

This poped up in my "google alert" today.

I don't really know waht to make of it.

 

Abnormal Proteins Linked To Schizophrenia Found In Body Tissue

Main Category: Schizophrenia News

Article Date: 24 Dec 2006 - 2:00 PST

 

A new study suggests biochemical changes associated with schizophrenia aren't limited to the central nervous system and that the disease could have more encompassing effects throughout the body than previously thought.

The findings, scheduled for publication in the January 2007 issue of the American Chemical Society's Journal of Proteome Research, could lead to better diagnostic testing for the disease and could help explain why those afflicted with it are more prone to type II diabetes, cardiovascular diseases and other chronic health problems.

. . .

After looking at thousands of proteins, they found that people with schizophrenia had 14 liver proteins and eight red blood cell proteins that were significantly altered compared to individuals who didn't have the disease.

. . .

Several of these abnormal proteins appear to promote oxidative stress and disrupt energy metabolism in cells,

Abnormal Proteins Linked To Schizophrenia Found In Body Tissue

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USA: Too slow to help, too eager to kill

Systemic failure and the execution of severely mentally ill offenders

 

Hundreds of severely mentally ill offenders in the US, are mired within a healthcare system that is too slow to help and a justice system that is too quick to pass death sentences

. . .

Scott Panetti, who was sentenced to death in Texas in 1995 for killing his parents-in-law in 1992. He has a long-documented history of hospitalization for his mental illness, including schizophrenia - which caused him visual and auditory hallucinations.

 

During his trial, Scott - who acted as his own lawyer dressed as a cowboy - said that demons had been laughing at him as he left the scene of the crime.

 

One of the doctors who was at the trial said: "...Scott was completely unaware of the effect of his words and actions. Members of the jury had hostile stares and looked at Scott in disbelief while he rambled and made no sense..."

 

Scott is still on death row.

Amnesty International Australia - USA: Too slow to help, too eager to kill

I wrote to the Governor of Texas about this kid. Never did get an acknowledgement or reply.

While the Psychiatrist said he had schizophrenia the jury disagreed.

Are all US Jurys that expert in metal Health? Amazing.

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Interesting articles but really the tip of the publication pile. Though there may well be an infectious etiology for certain variants of schizophrenia, I doubt it provides (or rather will provide) the all encompassing explanation we would like.

 

I suspect the truth is that is is one of the multifactorial diseases; the end point manifestation of several different disease processes that result in a common presentation and similar underlying pathology. A bit like hypertension, Rhumatoid arthritis, MS, reversible leukoencephalopathy etc., etc., A sort of meta-disease...

 

The variation from person to person will be dependent on genetics (and possibly geographical & social location), and etiological agents will include autoimmune/inflammatory, infectious, genetic, drug and toxin related. The presentation will lie on a spectrum depending on above as well as temporal factors. The relentless progression and underlying white/grey matter changes makes one suspect that many agents can light a particular fire, but once it's burning it can be difficult to halt..... The question is what fuels that fire once it's burning...

 

Without reading the original research articles it's difficult to add weight to the different arms of this disease. Another interesting fact about schizophrenia (and interest of mine) is that it seems to be possible to detect early disease by examining saccadic eye movements :shrug: ... Cool huh, the eyes are indeed the window to the soul :cup:

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Another interesting fact about schizophrenia (and interest of mine) is that it seems to be possible to detect early disease by examining saccadic eye movements ;) ... Cool huh, the eyes are indeed the window to the soul ;)

When nursing schizophrenic patients they seemed to have a certain"Look"

I have never heard of saccadic eye movements

Objective:Family studies have shown that abnormalities of smooth pursuit eye movement are increased in the adult relatives of schizophrenic probands as well as in the probands themselves. More recently, an inability of schizophrenic subjects to inhibit reflexive saccades reliably has been shown. This study aimed to test the hypothesis that the latter dysfunction is part of the extended schizophrenia phenotype
Saccadic Eye Movements in Families Multiply Affected With Schizophrenia: The Maudsley Family Study -- Crawford et al. 155 (12): 1703 -- Am J Psychiatry
Deficits in smooth pursuit eye movements are well documented in schizophrenia and schizotypic psychopathology. The status of eye tracking dysfunction (ETD) as an endophenotype for schizophrenia liability is relatively robust.
Entrez PubMed

 

I am not sure I understand what this means.

Can you explain in words of one sylable?

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The way we see is often split into to methods.

 

1) Saccadic eye movements. These are jumpy, start/stop movements. For example, you are looking at your computer monitor, but then the cat jumps on the table and you quickly focus on that. It's incredibly fast and "snappy." These movements happen all of the time, as we refocus the object of interest into our visual sweet spot.

 

2) Smooth pursuit movements allow us to track movement of the same object, like when you watch an ant crawling across the table. Instead of having to follow it with choppy "focus here, now focus there, now focus there" movements, you remain focussed and pursue it smoothly. :)

 

Jeff B. Pelz

The first job of an eye movement system is to move the eye quickly from the current point of gaze to a new location. Vision is blurred during an eye movement, so the length of time that the eye is moving must be minimized. In order to minimize the time during which no clear image is captured on the fovea, eye movements that move the fovea from one object/point to another are very rapid. These saccadic eye movements are among the fastest movements the body can make; the eyes can rotate at over 500 deg/sec, and subjects make well over one hundred thousand of these saccades daily. These rapid eye movements are accomplished by a set of six muscles attached to the outside of each eye. They are arranged in three pairs of agonist-antagonist pairs; one pair rotates the eye horizontally (left - right), the second rotates the eye vertically (up - down), the third allows 'cyclotorsion,' or rotation about the line of sight.

 

 

Some helpful visual graphics of the visual system on this .pdf. -- Specific to this topic would be data on page 10.

 

 

Pursuit movement - Wikipedia, the free encyclopedia

Pursuit movement is the ability of the eyes to smoothly follow a moving object. It is one of two ways that visual animals can voluntarily shift gaze, the other being saccadic eye movements. Pursuit differs from the vestibulo-ocular reflex, which only occurs during movements of the head and serves to stabilize gaze on a stationary object. Most people find pursuit extremely difficult, if not impossible, to initiate without a moving visual signal.
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While it is not the only factor, I've often felt that schizophrenia had some hereditary link involved with an individual's predispositional susceptibility. And complimenting this possibility, regressive genes may also be adding to the mix. As strange as it may sound, this thought occured to me one evening while watching a National Geographic special about wild life in Africa. The scene is set around a watering hole. Those animals stopping to drink appeared very nervous and paranoid. Needless to say, they had good reason because the lions are in the habit of taking advantage of these circumstances when catching their prey. It occured to me that overcautiousness displayed by we humans may be caused by a regressive gene memory from our distant past. Just thinking outloud............................Infy

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While it is not the only factor, I've often felt that schizophrenia had some hereditary link involved with an individual's predispositional susceptibility. And complimenting this prosibility, regressive genes may also be adding to the mix. As strange as it may sound, this thought occured to me one evening while watching a National Geographic special about wild life in Africa. The scene is set around a watering hole. Those animals stopping to drink appeared very nervous and paranoid. Needless to say, they had good reason because the lions are in the habit of taking advantage of these circumstances when catching their prey. It occured to me that overcautiousness displayed by we humans may be caused by a regressive gene memory from our distant past. Just thinking outloud............................Infy

Interesting thought. Paranoia as a useful genetic trait, especially when someone/everyone wants to eat you! I watched my crabs down at the lake yesterday. They were totally paranoid. they couldn't believe I had given them a free feed and keep scurrying into dark holes and rock crevasses.

(Reminder to self: local fish co-op has great crabs for sale at $10 a kilo- get some)

 

I am sure I read that there is a genetic basis to Schizophrenia.

I found this article on it but find it incomprehensible. Can anyone translate?

ScienceDirect - Biological Psychiatry : The origin of schizophrenia: genetic thesis, epigenetic antithesis, and resolving synthesis
Abstract

 

Traditionally, it has been thought that schizophrenia results from the interaction of predisposing genes and hazardous environmental factors.

In this article, the paradigm of “genes plus environment” is challenged, and a new interpretation is presented, in which the emphasis on DNA sequence variation is shared with epigenetic misregulation as a critical etiopathogenic factor.

Partial epigenetic stability (metastability) of gene regulation is consistent with various nonmendelian irregularities of schizophrenia, such as the presence of clinically indistinguishable sporadic and familial cases, discordance of monozygotic twins, coincidence of peaks of susceptibility with major endocrine rearrangements, and fluctuating course of disease severity, among others.

It is also suggested that stochastic epigenetic events might account for a substantial portion of phenotypic variance, which traditionally has been ascribed to environmental effects.

This theoretic essay is constructed according to the principle of Hegelian dialectic reasoning (thesis–antithesis–synthesis), which serves the goal of showing that the best outcome of molecular genetic studies in schizophrenia (and perhaps other complex diseases) can be expected when components that effect chromatin structure and gene regulation are taken into account and investigated comprehensively.

 

 

1) Saccadic eye movements. These are jumpy, start/stop movements.

I never noticed these in the Schizophrenics I nursed.; but they were doped up to the gills with tranquilisers. I noticed they just looked different. I couldn't put my finger on what. Perhaps not looking at you directly; perhaps a certain unhealthy "oiliness" look to the skin.

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The study above seems to basically be making a case for the idea that schizophrenia is not influenced by the environment, that it's all about the genes. They briefly describe their logic, and reference some specific genetic variables they deem important, but that's about as far as I get with it.

 

As for saccadic movements, note that these are not specific to folks with schizophrenia. All of us have saccadic movements. The study you referenced on the previous page seems to indicate that schiophrenics have more saccadic movements than a non-schizophrenic individual, and that if these saccadic movements were measured closely, they may provide an objective test of the phenomenon.

 

I'm not a doctor, but I read about one in a book once. :)

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I'm not a doctor, but I read about one in a book once. :phones:

lol

I watch "House" does that count?

 

I don't know if being adoctor really helps one understand this terrible mental disease that touches so many.

 

In the 1920's (?) half the schizophrenics in USA mental hospitals were "cured' when they put back the vitamin B that had been taken out of highly refined white bread. They had Pellagra, a vitamin B defincency.

As vitamin B is so important to the proper health of nerves & their firing (basically helping keep the "insulation' around them healthy -alcoholics get 'peripheral neuritus.') I often wonders if it would help Schizophrenia

It may be that schizophrenics cannot properly deal with Niacin

Clinical subtyping reveals significant differences in calcium-dependent phospholipase A2 activity in schizophrenia

. . .Significantly more schizophrenic patients were niacin-insensitive than controls (χ2(1) = 12.8, p < .001).

ScienceDirect - Biological Psychiatry : Clinical subtyping reveals significant differences in calcium-dependent phospholipase A2 activity in schizophrenia
Our data support the findings that absent response to niacin is more frequent in schizophrenic than in healthy individuals

ScienceDirect - Schizophrenia Research : Increased phospholipase A2 activity in schizophrenia with absent response to niacin

Twelve (42.9%) of 28 schizophrenic subjects did not vasodilate in response to a 200-mg niacin challenge dose, whereas only 1 of 18 (6%) bipolar disorder subjects and none of 28 controls showed impaired response
ScienceDirect - Biological Psychiatry : The niacin challenge test: Clinical manifestation of altered transmembrane signal transduction in schizophrenia?
Vitamin B12 and folate deficiency may contribute symptoms of disorientation, depression or psychosis; their measurement is a part of routine dementia work-ups. Pyridoxine deficiency results in seizures, although the effects of exogenously administered pyridoxine are not clearly understood in depression and anxiety - the disorders in which it is most frequently used clinically.

. .

The use of vitamins has been most prominent in psychiatry in the treatment of schizophrenia, where large doses of nicotinic acid were initially given alone and later combined with other vitamins and minerals. Several theoretical models were described to support the use of vitamins in schizophrenia. These included: the parallels of schizophrenia to the psychiatric symptoms of pellagra; hypotheses of a defect in adrenaline metabolism; and the accumulation of psychotoxic substances which produce psychotic symptoms.

. . .

trials failed to show efficacy for any of the vitamin therapies tested.

Entrez PubMed

 

I just found those few articles on the web.(Niacin-the one that makes you flush -is only available with a script. It is also used for high BP)

30 years ago I got a lousy grade in a Psychopathology paper from the psyciatrist running the course with a paper (own choice of subject) on Pellagra Vitamin B LSD and Schizophrenia. When I asked why, I was told "O if I thought B vitamins would help my patients. I would buy it by the truck full"- ever since I have disliked psyciatrists.

 

LSD too produces the same symptoms as Schizophrenia.

Do Schizophrenics produce their own LSD in the body as we do Opium and Canaboids?

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No, it's more to do with the brain region involved...(frontal and temporal, my two favourite)... Also the patterns of disease causality change with time. Sure, once you could explain several common psyc syndromes on a nutritional basis, but as these became less of a national issue (i.e standard of living increasing), so other, once rare, manifestations come to the fore. It's those tricky sticky statistics again.... mmmm patterns of disease.. (e.g. Syphilis, TB, heavy metal poisoning)

 

Very long rant on this to follow in a few weeks once i'm through these cursed exams (of which psyc is a component)...

 

Schizophrenia.com - Schizophrenia Pictures - Brain Disease Process

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No, it's more to do with the brain region involved...(frontal and temporal, my two favourite)... Also the patterns of disease causality change with time. Sure, once you could explain several common psyc syndromes on a nutritional basis, but as these became less of a national issue (i.e standard of living increasing), so other, once rare, manifestations come to the fore. It's those tricky sticky statistics again.... mmmm patterns of disease.. (e.g. Syphilis, TB, heavy metal poisoning)

 

Very long rant on this to follow in a few weeks once i'm through these cursed exams (of which psyc is a component)...

 

Schizophrenia.com - Schizophrenia Pictures - Brain Disease Process

I look forward to the rant. good luck in the exams

 

I am not so sure that we still don't have nutritional aused disease in the west. finding figures on this is hard because they mainly deal with developing countries. I will see what i can find

 

This was interesting

Dr. Paul Fink, past president of the American Psychiatric Association, has acknowledged that every psychiatric disorder in the Psychiatric Diagnostic Symptoms Manual IV (DSM-!V) can be caused by Lyme Disease.

and parasitic disease

Conventional medical practice in the United States largely ignores the possibility of parasitic disease.

. . .

Three weeks after eliminating her infection she was no longer depressed, her exhaustion was gone and her zest for life had been restored.

This is very common I think

To make the proper diagnosis of psychiatric symptoms even more complex it is now well established that the overgrowth of candida (yeast) organisms, fungi, mycoplasma, and dangerous anerobic organiasms in the intestinal tract after antibiotic therapy, high sugar intake, and illnesses which injure the lining of the intestine can cause impaired brain function (seizures, confusion, poor memory, depression, learning difficulties, headaches and short attention span). These brain symptoms are caused by absoption of neurotoxic substances produced by mycoplasma, fungi, borrelia, yeast and anerobic organisms.

These neurotoxic substances also commonly cause injury to the hypothalamus which leads to impaired production of endocrine hormones. Therefore, patients with intestinal pathogen overgrowth often manifest impaired function of the thyroid gland (hypothyroidism) and adrenal insufficiency (Addison's Disease).

Every second person seems to have Herpes Simplex Type 2

Research done at Johns Hokins Children's Center and published in the Archives of General Psychiatry in 2001 disclosed that mothers with evidence of Herpes Simplex Type 2 infection during pregnancy were 6 times more likely to have a child who later developed schizophrenia than mothers without herpes infections.

One scary article- but well worth reading in full

Parasitic infections which invade the brain (neurocysticerccosis) manifest depression and psychosis in more than 65 % of cases.

Dr. James Howenstine -- The Overlooked Relationship Between Infectious Diseases And Mental Symptoms

We don't have lyme disease in OZ, but some suspect we have something similar- but no pathology tests for it

 

 

I don't think you should mention any of this in your exams???

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  • 1 month later...

schizophrenia

Schizophr Res. 1997 Feb 28;23(3):253-7.

Borna disease virus antibodies and the deficit syndrome of schizophrenia.

 

Waltrip RW 2nd, Buchanan RW, Carpenter WT Jr, Kirkpatrick B, Summerfelt A, Breier A, Rubin SA, Carbone KM.

 

Maryland Psychiatric Research Center, Department of Psychiatry, University of Maryland at Baltimore, Catonsville 21228, USA.

 

We detected anti-Borna disease virus (BDV) antibodies at a 14.4% rate in patients with schizophrenia. The hypothesis of a higher rate of BDV seropositivity in deficit syndrome was borne out in a subset of 64 patients categorized according to the Schedule for the Deficit Syndrome with 5/15 seropositive deficit and 4/49 seropositive nondeficit (p < 0.05). This suggests that the antibodies and possibly a BDV-like virus are pathogenetically linked to this form of schizophrenia.

Entrez PubMed

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http://www3.interscience.wiley.com/cgi-bin/abstract/114112711/ABSTRACT?CRETRY=1&SRETRY=0

Abstract

HOPA (MED12) is an X-chromosome gene that codes for a critical member of the Mediator Complex, a group of proteins that regulates transcription via the nuclear receptor, Wnt and Receptor Tyrosine Kinase pathways.

In prior association and meta-analyses, we have shown that the presence of an evolutionarily conserved, 12 bp (4 amino acid) insertional polymorphism in exon 43 of this gene is associated with increased risk for an endophenotype of schizophrenia. In this communication, we describe the results of our work with subjects and data from the National Institutes of Mental Health (NIMH) Genetics Initiative for Schizophrenia.

We report that the presence of the HOPA12bp polymorphism is associated with increased risk for schizophrenia in subjects of European ancestry.

In the light of this new study and the prior wealth of clinical and basic science data, we conclude that the HOPA12bp allele is a risk factor for schizophrenia in subjects of European ancestry and suggest that further studies to define the endophenotype and mechanisms of illness associated with this polymorphism are indicated. © 2007 Wiley-Liss, Inc.

Received: 18 August 2006; Accepted: 27 November 2006

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