How Schizophrenia Affects the Brain

[SMM]

It seems there are some who can live for years, or a lifetime, without exhibiting any real sign of suffering or having it affect their lives. Since it doesn't rock the boat or interfere with their comfort or self-interest, exploration doesn't cross their minds when the opportunity presents itself.

Sorry to hear about your mum & aunt also H-kqge.

Too true. Although i do see people around me disintegrating but it seems as though the mere thought of giving up cakes & pizzas & fizzy crap sends a signal to part of their mind that says "do not entertain notions of giving up sweet-tasting goods." Definitely a case of "being killed by comfort."
Just to be clear for your autism post SMM, & my earlier post in this thread, my mother is the eldest of 4 sisters & my youngest aunt got the "mental illness" first, then my mother 5 years back. The other 2 are twins & one of them told me of a discussion they had about feeling like they were "going mad." (their words)
And this is when it actually happened to my mum. My mum was officially diagnosed as wheat-gluten intolerant (dunno if they couldn't make their minds up, it's supposed to be one or the other isn't it?) in 2000/2001 which aided my correlations but alas, it means squat to them. I can only look after me now & it's their choice, especially my grandmother (they're all Christians with the usual prejudices) who just loves to say "God will solve it." Because we're special probably. Thanks for your concern.

Just to clarify, when you say "mental illness", do you mean schizophrenia or autism?

The "God will solve it" resolve is the same in my mum's - it's indoctrinated down her family line. Her side of the family also exhibit autism-related disorders, developmental issues, sickle cell trait-anaemia & deaths have occurred on her side of the family related to this [i.e. retardation, autism, schizophrenia, other neural anomalies]. The chance it's genetically transferred is highly likely.

Trouble is, coming from a rural background where medical support was [& still is] costly & questionable at best, I'm not sure how educated they are on the matter. Maybe when these things were taking place generation after generation, the most fitting resolution was to rely on religion - now it's simply at the point where all faith is placed there despite alterations in external environment?
If it wasn't for reading or looking into the matter, changing diet & sorting through 'the past' [or trying], I don't think anyone would have turned around & pointed this - the possibility of me being on the autistic-spectrum & genetic transmission which could qualify as evidence - out. Considering how neatly it fits with past & present experiences it's a little bewildering.

Knowing makes a difference osit. I agree with your point of looking after yourself. When someone else suffers enough [I wouldn't wish it on anyone but it's a strange fact of physical existence] & acts accordingly, they are then presented with a choice - with the knowledge that the option is there.

This is disconcerting news. As my LD gf is suffering from untreated(by her own choice) schizophrenia it is important to find any and all supportive modes of treatment.

It has long been a suspicion that antipsychotic meds damage the brain in some way but so far its has never been clear whether the observed changes are due to the illness itself or to the medication. This study apparently shows it is both.

Perhaps there is a link between infection/inflammation and early brain development?

To add to the resources provided, here is a talk by Eleanor Longden: http://www.youtube.com/watch?v=syjEN3peCJw

She tells the story of how she was diagnosed with schizophrenia and how she changed and was changed by it.

She makes some worthwhile points on the psychiatric side of things imo - interesting to watch.

Incredible to think that people with Schizophrenia might not only "do better" with a change of diet and the taking of certain supplements - but could also potentially thrive in ways, perhaps, that people without this condition can.

Thanks Ennio for sharing the session excerpts & Hoffer's anecdote journal entry. I'm going to re-read them properly later on in the day/tomorrow.

 

[H-KQGE]

Apologies SMM, i meant that my mum is schizophrenic & that my youngest aunt who got "mentally ill" has never been diagnosed with anything specific, to my knowledge. Since their mother looks after all their affairs legally, (she's an official carer & receives money for it) & refuses outright that none of her children are "mad", (her words) then i doubt she would reveal info confirming it. It's because i lived with my mother from age 10 up until 5 years ago that i know her behaviour so well. The subtle probing about family history (asking one aunt & my grandmother ) began around then, but certain issues were obviously too much - primarily the mental health one. A lot of the time my grandmother will just scream at my mother &/or aunt when they won't "behave", which is doing as they're told in terms of (even more) praying to God/Jesus, & eating more fruit & veg (as well as still eating junk that has propelled formerly slim women into obese ones who have rapidly gained around 20 years on their faces, when the family trait was very youthful looks) as she loves to tell them.

I've only been able to keep up with Schizophrenia, (mother) Parkinson's, (crops up a lot in neuro-biological research) & Huntingdon's (my friend's wife & her family) but i don't have enough to go on where my youngest aunt is concerned. I'll start paying more attention to autism though. Here's some of what i've seen :

http://www.autism.com/index.asp

Of course you'll look around & do your own thing, i started off with "Summary of Dietary, Nutritional and Medical Treatments for Autism." A pdf is at the bottom, or you can grab it now :http://ariconference.com/enews/treatment.pdf

I used the 1st link in the pdf to go to aspergers specifically (i've already learned a lot about the histories & differences between Aspergers & Autism, it's encouraging) & there's other stuff on heavy metals & digestive enzymes & more. You'll probably recognize some things that the forum has covered already as well, but i found it useful since i knew very little. As you'll see, there's loads to sink your teeth into from there. Again, thanks.

 

[clearmiddle]

...Of course you'll look around & do your own thing, i started off with "Summary of Dietary, Nutritional and Medical Treatments for Autism." A pdf is at the bottom, or you can grab it now :http://ariconference.com/enews/treatment.pdf

I find this interesting, as someone who has been self-treating Asperger's for quite a few years. When I looked at these types of guides in the past, I found them confusing and not very helpful. This is more the kind of information I can use. Thanks!

I used the 1st link in the pdf to go to aspergers specifically (i've already learned a lot about the histories & differences between Aspergers & Autism, it's encouraging) & there's other stuff on heavy metals & digestive enzymes & more. You'll probably recognize some things that the forum has covered already as well, but i found it useful since i knew very little. As you'll see, there's loads to sink your teeth into from there. Again, thanks.

I didn't find anything about Asperger's at that website. Perhaps it has been removed? There was one link for a PDF, but it led only to "page not found."

 

[H-KQGE]

I didn't find anything about Asperger's at that website. Perhaps it has been removed? There was one link for a PDF, but it led only to "page not found."

Ok Megan, i tried the same process as you quoted again, i went into the pdf & used the 1st clickable link - http://autism.asu.edu (i just tried to hyperlink it but i see what you mean. The same link in the pdf worked for me as i've just tried it - a few times) the link in the pdf was written with regular brackets around the address - it works from there but not here, removing it though, links correctly. Anyway...

Just in case anyone else has issues with the same thing the pdf has a link "(for asperger's see www.autism.com)" which is the same as the 1st clickable link in my original post. You'll be taken to the ARI (Autism Research Institute) homepage. To clarify, if looking for Aspergers click the first hyperlink in this post for ease. When at the ARI homepage you can type "aspergers research" into the search bar & your returns are three clickable links.
1."Successful Independent Living" (decent enough)

2. "Education and Aspergers Syndrome" (better, talks about Aspergers being "an intact population & that it's a diagnostic group independent of any other group that falls on the spectrum of Autism.")
3."An Interview with Richard L. Simpson. Ed. D" (one of the pioneers in the education of Autism & Aspergers Syndrome apparently) This third one didn't work for me, it linked back to the ARI homepage, it might work for others though.

I actually started off in the "latest research" section with the link i gave about the dietary nutritional info. The FAQ section containing the "DSM - V: What the Changes May Mean" (Diagnostic & Statistical Manual - Fifth Edition) is interesting as it talks about the revision of the diagnostic criteria for Autism that eliminate the diagnosis of Aspergers & so on. There's a video embed on the page too.

Returning to the asu link (Arizona State University) which carries the "Autism/Aspergers research program" page, if you click the "Greater Phoenix Chapter" link (about prof. Adams) then click "Understanding Autism" (at the very top of the page, but you can't enlarge the page with double-click zooming, Megan i think you said somewhere about your eyesight, so it's the 2nd underlined title next to "home" in the top left of the screen) then "Aspergers 101." (scroll down a bit)
You should see some decent info, although you may have some of it already. For me, there are links about Aspergers that get a definite tick, & the book references at the bottom seem especially useful. Since i was raised exclusively by women, i'm always more aware of women oriented health info regardless if my relatives won't help themselves. So on that note, here are the books on Aspergers that jump out at me:

*"A complete guide to Aspergers Syndrome" by Tony Attwood, PhD.

*"Kids in the Syndrome Mix of ADHD, LD, Aspergers, Tourette's, Bipolar, And More! :The One Stop Guide for Parents, Teachers, and Other Professionals" by martin L. Kutscher, MD.

*"The Oasis Guide to Aspergers Syndrome: Completely Revised and Updated Advice, Support, Insight, and Inspiration" by Patricia Romanowski Bashe and Barbara L.Kirby; Forewards by Simon Baron-Cohen,PhD and Tony Attwood, […] (i've read a bit on these 2 guys & their work seems good)

*"Women from Another Planet? Our Lives in the Universe of Autism" by Jean Kearns Miller ( collection of writings by women on the autism spectrum )

*"Aspergers Syndrome in the Family: Redefining Normal" by Liane Holliday Willey

*Aspergers Syndrome and Long-Term Relationships" by Ashley Stanford

*"High-Functioning Individuals With Autism" (Current Issues In Autism) by Eric Shopler, gary B. Mesibov

*"Autism and Aspergers Syndrome" by Uta Frith (Editor) The translation of the original Hans Asperger paper.

It seems that the medical mafia "did him" like they did to Tesla where his pioneering work is concerned, though not as bad. There's more as you'll see, & that's page 1, page 2 is to do with teenagers & felines pages 3 & 4 are duds. Back to the ASU Aspergers page. All of the titles are "downloadables" or links to other places that are Autism related. I've checked the links for the "Upcoming Events" part & the spring conference info one is a dud, but the rest seem fine.

In the 4th page of that original pdf link (dietary, nutritional etc) there's also a link for ACAM - American College For Advancement In Medicine (www.acamnet.org) again, typing in "Aspergers research" in their search bar gives almost 20 results. So now i have almost 40 to check out! Hope everything works for you this time.

 

[H-KQGE]

This sounds good. More of an update really.My interest is in the visual processing in terms of how humans actually see. Which is always worth remembering.
http://www.vancouversun.com/health/Schizophrenia+finding+could+lead+therapy+early+diagnosis+research/8974720/story.html

VANCOUVER -- New research at the University of British Columbia on the role of visual processing in schizophrenia could open the door to earlier diagnosis of the illness and potential therapies.

“(Schizophrenics) may have difficulty with the simplest tasks like crossing the street safely, reading a map or using the correct change on the bus,” said Miriam Spering, lead author of a recent article in the Journal of Neuroscience. “It occurred to me that many of those problems may be visual.”

Schizophrenia is a common mental illness characterized by disordered thoughts and speech, delusions and often, auditory and visual hallucinations. It affects about one person in 100, usually manifesting between the ages of 15 and 35.

Patients struggle with simple visual tasks such as tracking a moving object in a video game and predicting its movements compared with normal subjects tested by Spering. “What we found was a bit of a surprise,” she said.

Impaired eye movement long known to be associated with the illness is not sufficient to explain the difference in performance.

Much of what we see is “constructed” by the brain, which integrates visual information from the eyes with a predictive image generated by the brain to confirm visual information, fill in gaps and process the motion of objects, she explained.

When schizophrenics fail to integrate the two images and the information in the brain conflicts with eye movements, their world is neither stable nor predictable.

Spering is optimistic that her finding will lead to a therapy to alleviate visual symptoms of schizophrenia.

“If we can understand what is going on in their brains we can start developing therapeutic tools based on vision and eye movement,” she said.

Spering is now expanding on her original research, studying the abilities of athletes with better-than-normal visual motion processing abilities.

At the request of UBC’s baseball coach Terry McKaig, Spering is observing his players’ eye movements while they hit balls in a batting cage in hopes of creating a program to improve hand-eye coordination for daily use by his athletes. What she learns could benefit schizophrenics, too.

“It is my vision to develop an easy-to-use tool that can be used by any patient to improve their eye movements,” she said.

She will soon begin examining the families of schizophrenics with the goal of finding genetic clues that could help predict who is likely to become schizophrenic.

“We are going to extend the study now to the relatives of known psychotics to see if they have similar impairment, which would suggest a strong genetic component (to schizophrenia),” she said. “Hopefully, in the future, we may be able to use this as a sensitive early marker for the disease.”

I just hope that they implement some necessary tests on the athletes health, rather than the simple approach that they might take, which the article seems to suggest.

There is a video that may add more, it requires Adobe flash player (which I don't have) to watch it though.

 

[H-KQGE]

I'm not sure if this is ground-breaking as this piece claims, it's 2013 for crying out loud.
http://www.theaggie.org/2013/10/03/pregnant-mothers-immune-systems-contribute-to-autism-in-children/

Pregnant mothers’ immune systems contribute to autism in children
Susceptibilities To Viral Infection During Pregnancy Increases Risk Of Having Autistic Children

Written By JASBIR KAUR
Aggie Science Writer
Published On October 3, 2013
Filed Under Science & Technology

Autism and schizophrenia diagnoses are at an ultimate peak.Fortunately, a recent study published in the Journal of Neuroscience and conducted within the UC Davis Center for Neuroscience and Department of Neurology offers groundbreaking research about these neurodevelopmental disorders. Lead author of the study Kimberley McAllister, a professor and a researcher at the UC Davis MIND Institute, suggests that the risk of having a child with autism or schizophrenia might be higher if a pregnant mother contracts a viral infection.

The study is the first of its kind to help scientists understand how maternal immune activation affects a newborn’s neuronal and synaptic development.

“Our research indicates that immune molecules on neurons in the developing brain, control the formation of connections, and that process can be altered by a peripheral immune response during gestation,” McAllister said in an email.

The study focused on MCHI molecules — immune molecules found in the brain. McAllister and her team injected pregnant mice and rats with poly(I:C), a double-stranded RNA synthetic which mocks a real viral infection and tricks the immune system of the rodents. Thus, it activates their system without actually infecting the animals.

Myka Estes, a fifth-year graduate student in McAllister’s lab, gave the following comment regarding her interest in this field of research.

“I was diagnosed with an autoimmune disorder and experienced cognitive complications from the disease,” she said. “This experience piqued my interest in how maladies of the immune system can affect brain function.”

The team used two test groups of rodents. In one group, the animals’ immune system was activated, and in the other, it was not. The newborns of the animals who were treated with the poly(I:C) viral infection showed greater levels of the MHCI molecules found in the brain. Similarly, in the group whose immune systems remained inactive, the levels of immune molecules did not show significant changes. Such a method helped the researchers report for the very first time that high levels of MHCI impairs neuronal ability from the newborns’ brains to form synapses — chemical signals that pass between nerve cells. The team was also able to identify the first molecular pathway of MHCI molecules, which aids in synaptic regulation.

Though contracting a viral infection while pregnant is a risk factor for having a child with autism, it still is only a risk — and not a guarantee — that a child will develop autism. According to Judy Van De Water, a professor and director of the UC Davis Center for Children’s Environmental Health, a subset of the population is likely to have an increased risk of developing autism.

“Boys are at an increased risk over girls, and siblings of an affected child are at increased risk by 20 percent,” said Van De Water.

With the flu season coming up, pregnant mothers all around are warned to be cautious. As far as the study is concerned, the results are promising, yet it is only the first step in improving interventions for developmental disorders.

Research isn’t the only way in improving the lives of children with autism and their families. Kirkland Washington III, a behavioral therapist at Capitol Autism Services and a 2012 UC Davis graduate, shares his experience with working with children with autism.

“Patience is extremely essential and an understanding that who you are working with won’t necessarily understand what you’re asking of them or be able to communicate their wants or needs at the time,” he said.

With the help of research and altruistic people combined, there seems to be hope to make these disorders less prevalent.

You just know they're gonna bang extra hard on that "get yer flu jab" drum.

 

[SeekinTruth]

You just know they're gonna bang extra hard on that "get yer flu jab" drum.

That was the suspicion in my mind while reading the article. I find it hard to believe that the opportunity to drive that message very hard would be missed.

 

[H-KQGE]

This study is on the first molecular genetic test to determine if genetic markers of reduced cognitive ability were also genetic markers of increased schizophrenia risk.

_http://www.eurekalert.org/pub_releases/2013-12/nsij-fir121613.php

Feinstein Institute researchers show a genetic overlap in schizophrenia and cognitive ability

MANHASSET, NY – Investigators at The Feinstein Institute for Medical Research have discovered for the first time, direct evidence of a genetic overlap between schizophrenia and general cognitive ability. The findings are published online in Molecular Psychiatry.

Schizophrenia is a chronic, severe and disabling brain disorder that affects approximately 2.2 million Americans each year. It is characterized by a significant reduction in general cognitive abilities, so that many patients struggle with completing school, holding jobs and achieving their full potential. Previous studies have indicated subtle cognitive abnormalities in undiagnosed and unmedicated relatives of patients who live with schizophrenia, which suggests the possibility of genetic overlap between risk for schizophrenia and cognitive traits. These previous studies, however, did not test this overlap on the molecular level.

Anil Malhotra, MD, director of psychiatry research at Zucker Hillside Hospital and an investigator at the Feinstein Institute, and his colleague Todd Lencz, PhD, associate investigator at the Zucker Hillside Hospital and the Feinstein Institute, conducted the first molecular genetic test to determine if genetic markers of reduced cognitive ability were also genetic markers of increased schizophrenia risk.

Specifically, they conducted a large-scale, meta-analysis, genome-wide association study (GWAS) of samples from 5,000 subjects provided by the Cognitive Genomics consorTium (COGENT). COGENT, which was founded and is led by Dr. Malhotra, is an international consortium of nine teams of researchers across seven countries. Through their analysis, they confirmed that patients who suffered from schizophrenia also had lessened cognitive ability. This is the first direct evidence for genetic overlap between schizophrenia risk genes and genes that regulate general cognitive ability, such as memory, attention, and language abilities. The results provide molecular confirmation of this genetic overlap and additional insight into how schizophrenia develops and progresses.

"This research leads us to a deeper understanding of how schizophrenia affects the brain at the molecular level," said Dr. Lencz. "Our studies are designed to provide clues to the development of new treatments to improve the lives of our patients."

 

[Buddy]

[quote author=article]
"This research leads us to a deeper understanding of how schizophrenia affects the brain at the molecular level," said Dr. Lencz. "Our studies are designed to provide clues to the development of new treatments to improve the lives of our patients."

[/quote]

Anyone interested in subjects like schizophrenia as well as other mental illness and the human genes connection, may also be interested in understanding a couple of related ideas, like why researchers focus primarily, or only, on genes, the continuing arguments over whether behavior is inherited or acquired and the background context: the medical "machine" model.

For understanding these connections, I found the following conceptual paper and its conclusion fascinating:

Trivial and non-trivial Machines in the Animal and in Man
Georg Ivanovas, (with an extensive Bibliography)


Keywords: genes and behaviour, recursivity, non-trivial machines, Heinz von Foerster

Paper type: Conceptual paper

Purpose of this paper: It was the aim to apply basic epistemological concepts, as presented by Heinz von Foerster, to current problems of medicine and biology.

Design: The relation of genes and human behaviour is an important issue in current medical discourse. Many states and diseases are claimed to be caused by a genetical disposition. To prove the soundness of such claims, a strict methodology has to be applied.

Findings: The usual approach of combining genetical findings with observed behaviour is based on an insufficient epistemology. The neglect of recursive processes leads to misinterpretations that have far-reaching consequences, especially if disease and therapy are concerned.

Implications: A precise analysis of recursive traits would allow more reliable models of the relation between genetical disposition and environmental influence.
What is new: The paper reflects trivial or non-trivial relations in social behaviour that are often neglected.


The situation

In recent years there has been an increasing number of publications proving that behaviour has a genomic cause. The Science magazine classified the understanding of this relation as the second ranked breakthrough of the year 2003 with the promising title “Decoding mental illness” (Science news and editorial staffs, 2003). But this issue is not new. It has been discussed in psychiatry for many years in the search for the cause of schizophrenia - today correlated with a variety of genes (Harrison & Owen, 2003). However, if we open a medical journal, especially Molecular Psychiatry, we find that a lot of behavioural patterns are reduced to genetic causes. Here are some arbitrary examples:


There is a strong connection between ADHD (attention-deficit hyperactivity disorder – diagnosed according DSM-IV) and the allele 4-repeat of the IL-1 RA gene, coding Interleukin-1 antagonists, whereas the allele 2-repeat is associated with a reduced risk (Segman et al, 2002.).
There is a significant linkage of ‘simple phobia’ to chromosome 14 markers (Gelernter et al., 2003).

The Grp-gen is regulating ‘Pavlovian learned fear’ by influencing the lateral nucleus of the amygdala (Shumyatsky et al., 2002).

Individuals with one or two copies of the short (s-) allele of the 5-HTT gene are much more likely to develop depression than individuals with the long (l-) allele when confronted with emotional stressors between the age of 21-26 (Caspi et al., 2003).


Of course this is the resumption of the old discussion whether behaviour is inherited or acquired. Already in 1960s fierce quarrels erupted on this subject. Results have been forged (Di Trocchio, 1993), professors have been beaten, in short: real life roared around this issue.

Since then, some decades have passed, and science has made incredible progress. Not only has the genetic research made progress, but knowledge and understanding of (self) organisation of life have been successful as well. It was especially Heinz von Foerster and the members of his Biological Computer Lab (BCL), Maturana, Ashby and Günther, just to name a few, who influenced these ideas.

Revisiting some of these ideas gives us the tools to judge whether the findings of genomic behaviourism are sound and to what extent they can be helpful as to the understanding of the mechanisms of disease.

See Ivanovas G (2005): Trivial and non-trivial machines in the animal and in man, Kybernetes 34; 3-4: 508-520 or a web link here:
_http://www.ivanovas.com/english/kybernetes.html

 

[H-KQGE]

Adding more to the puzzle of schizophrenia, this time retrotransposons.

Jumping DNA in the brain may be a cause of schizophrenia
27 December 2013

Stretches of DNA called retrotransposons, often dubbed “junk DNA”, might play an important role in schizophrenia. In a study published today in the journal Neuron, a Japanese team revealed that LINE-1 retrotransposons are abnormally abundant in the schizophrenia brain, modify the expression of genes related to schizophrenia during brain development, and may be one of the causes of schizophrenia.

Retrotransposons are short sequences of DNA that autonomously amplify and move around the genome. One class of retrotransposons named Long Interspersed Nuclear Elements (LINE) make up a large part of the eukaryotic genome and it is believed that they may contribute to a number of disorders and diseases such as cancer.

LINE-1 have been shown to be more abundant in brain cells than in other cells in the body in adults, providing evidence for enhanced activity of LINE-1 in the human brain. However, the role played by LINE-1 in mental disorders, and in particular schizophrenia, has remained unclear.

The team led by Dr Kazuya Iwamoto from the University of Tokyo and Dr Tadafumi Kato from the RIKEN Brain Science Institute demonstrated that the number of LINE-1 copies is elevated in the post-mortem brains of patients with schizophrenia. They show using mouse and macaque models for schizophrenia and iPS cells that exposure to environmental risk factors during development, as well as the presence of genetic risk factors for schizophrenia, can lead to increased levels of LINE-1 in neurons. The authors reveal employing whole genome analysis that in schizophrenia patients LINE-1 reinserts into genes involved in synaptic function or schizophrenia and may result in disruptions in their normal functions.

“Our findings strongly suggest that abnormal, enhanced retrotransposition of LINE-1 in neurons, triggered by environmental factors and/or combined with a genetic risk factor, plays a defining role in schizophrenia,” conclude the authors.

“This study proposes a brand new mechanism of pathophysiology of schizophrenia. Previously, schizophrenia was regarded as a disease caused by gene-environment interactions, but our study shows that the environment can alter the genome and may contribute to the disease,” explains Tadafumi Kato.

I don't know about that cancer part, maybe one of the contributors on the "what causes cancer?" thread can give an assessment; if it's a worthy addition to the information there. The fungal bacterial connections are all I can agree on with my limited knowledge.

 

[SeekinTruth]

From what I've read, epigenetic/gene expression effects from diet and environment (including all sorts of toxicity) regulate the genome to a very large degree. That percentage of DNA (in the 90's percentage) of non-protein coding "junk DNA," turns out to play all sorts of roles in what's going on with physical and mental health (and probably includes things not even on mainstream science's radar).

There's material showing that there's a large amount of viral DNA (from retroviruses) in humans and some are related to cancer and stem cells. So if the signals / information feedback with the overall environment changes so that cancer, among many other things, manifests, it seems plausible to me, for what that's worth.

The amount of retrotransposons being "anomalous" in schizophrenics also seems to confirm what the C's have said. Paraphrasing: that a person with shamanic genetics on the wrong diet becomes a schizophrenic. Basically, they might "see into other realms," or whatever, but can't do anything with it. It can't be used to help their people like the traditional shaman would use the information accessed in other realms.

 

[H-KQGE]

More on the errors in visual perception of schizophrenics. This time a "corollary discharge dysfunction" has been identified as a possible cause for some of the common symptoms. It sounds like an information/stimuli overload occurs when they have to focus.

https://www.mcgill.ca/channels-contribute/channels/news/noisy-brain-signals-how-schizophrenic-brain-misinterprets-world-234679

Noisy brain signals: How the schizophrenic brain misinterprets the world
News
PUBLISHED: 2 APR 2014

People with schizophrenia often misinterpret what they see and experience in the world. New research provides insight into the brain mechanisms that might be responsible for this misinterpretation. The study from the Montreal Neurological Institute and Hospital – The Neuro - at McGill University and McGill University Health Centre, reveals that certain errors in visual perception in people with schizophrenia are consistent with interference or ‘noise’ in a brain signal known as a corollary discharge. Corollary discharges are found throughout the animal kingdom, from bugs to fish to humans, and they are thought to be crucial for monitoring one’s own actions. The study, published in the April 2 issue of the Journal of Neuroscience, identifies a corollary discharge dysfunction in schizophrenia, which could aid with diagnosis and treatment of this difficult disorder. It was carried out in collaboration with researchers Veronica Whitford, Gillian O’Driscoll, and Debra Titone in the Department of Psychology, McGill University.

“A corollary discharge is a copy of a nervous system message that is sent to other parts of the brain, in order to make us aware that we are doing something,” said Dr. Christopher Pack, neuroscientist at The Neuro and lead investigator on the study. “For example, if we want to move our arm, the motor area of the brain sends a signal to the muscles to produce a movement. A copy of this command, which is the corollary discharge, is sent to other regions of the brain, to inform them of the impending movement. If you were moving your arm, and you didn’t have the corollary discharge signal, you might assume that someone else was moving your arm. Similarly, if you generated a thought, and you had an impaired corollary discharge, then you might assume that someone else placed the thought in your mind. Corollary discharges ensure that different areas of the brain are communicating with each other, so that we are aware that we are moving our own arm, talking, or thinking our own thoughts.”

Schizophrenia is a disorder that interferes with the ability to think clearly and to manage emotions. People with schizophrenia often attribute their own thoughts and actions to external sources, as in the case of auditory hallucinations. Other common symptoms include delusions and disorganized thinking and speech.

Recent research has suggested that an impaired corollary discharge can account for some of these symptoms. However, the nature of the impairment was unknown. In their study, Dr. Pack and his colleagues (including Dr. Alby Richard, neurology resident at The Neuro) used a test called a perisaccadic localization task, to investigate corollary discharge activity. In this test, subjects are asked to make quick eye movements to follow a dot on a computer screen. At the same time they are also asked to localize visual stimuli that appear briefly on the screen from time to time. In order to perform this task accurately, subjects need to know where on the screen they are looking – in other words they use corollary discharges signals that arise from the brain structures that control the eye muscles.

The results showed that people with schizophrenia were less accurate in figuring out where they were looking. Consequently they made more mistakes in estimating the position of the stimuli that were flashed on the screen. “What is interesting and potentially clinically important is that the pattern of mistakes made by the patients correlated with the extent of their symptoms,” said Dr. Pack. ““This is particularly interesting because the circuits that control eye movements include the best-understood structures in the brain. So we are optimistic that we can work backward from the behavioral data to the biological basis of the corollary discharge effects. We have already started to do this with computational modeling. Mathematically we can convert the corollary discharge of a healthy control into the corollary discharge of a patient with schizophrenia by adding noise and randomness. It is not that people with schizophrenia have no corollary discharge, or a corollary discharge with delayed or weaker amplitude. Rather the patients appear primarily to have a noisy corollary discharge signal. This visual test is very easy thing to do and quite sensitive to individual differences. “

The study shows that patients with schizophrenia make larger errors in localizing visual stimuli compared to controls. These results could be explained by a corollary discharge signal, which also predicts patient symptom severity, suggesting a possible basis for some of the most common symptoms of schizophrenia.

This work was supported by The Natural Sciences and Engineering Research Council of Canada, The Brain & Behavior Research Foundation (NARSAD) and the EJLB Foundation.

 

[H-KQGE]

I think that there's a fair amount of crossover from the study in this article. Neurons in the thalamic reticular nucleus (TRN) the "switchboard" direct sensory signals such as vision from the outside world, and internal information such as memories, to their appropriate destinations.

http://www.newswise.com/articles/researchers-identify-a-brain-switchboard-important-in-attention-and-sleep

Researchers Identify a Brain “Switchboard” Important in Attention and Sleep
Study bolsters understanding of brain circuit and points to new targets for treating psychiatric disorders

Citations
Cell

Newswise — New York City, August 14, 2014 - Researchers at NYU Langone Medical Center and elsewhere, using a mouse model, have recorded the activity of individual nerve cells in a small part of the brain that works as a “switchboard,” directing signals coming from the outside world or internal memories. Because human brain disorders such as schizophrenia, autism, and post-traumatic stress disorder typically show disturbances in that switchboard, the investigators say the work suggests new strategies in understanding and treating them.
In a study to be published in the journal Cell online Aug. 14, a team led by Michael Halassa, MD, PhD, assistant professor of psychiatry, neuroscience and physiology, and a member of the NYU Neuroscience Institute, showed how neurons in the thalamic reticular nucleus (TRN) — the so-called switchboard — direct sensory signals such as vision from the outside world, and internal information such as memories, to their appropriate destinations.
“We have never been able to observe as precisely how this structure worked before,” says Dr. Halassa. “This study shows us how information can be routed in the brain, giving us tremendous insight into how it might be broken in psychiatric disorders.”

For the study, researchers used a multi-electrode technique to record the activity of individual neurons in the TRN, a thin layer of nerve cells that covers the thalamus, a structure in the forebrain that relays information to the cerebral cortex, the seat of higher-level functions such as learning and language. TRN cells are known to send inhibitory signals to the thalamus, determining which information is blocked.
The activity of TRN cells, the researchers found, depended on whether the mouse was asleep or awake and alert. TRN cells that controlled sensory input were far more active during sleep, particularly during the periods of sleep when brief bursts of fast-cycling brain waves, called spindles, occur. Sleep spindles, which are associated with blocking sensory input during sleep, are known to be diminished among people with autism and schizophrenia.
Dr. Halassa says the new findings suggest that faulty TRN cells may be disrupting the appropriate filtering of information in these conditions. His group is now exploring this filtering process in animal models of schizophrenia and autism.
In experiments with alert mice, Dr. Halassa’s group found that sensory TRN cells fired very little. This suggested that while these neurons block the flow of external information during sleep, they facilitate the flow of information when an animal is awake and alert.
By contrast, TRN cells that control the flow of internal signals behaved in an opposite fashion, firing very little in sleep. This lowered level of activity, Dr. Halassa suspects, may allow memories to form, which is known to occur during sleep. The thalamus has nerve connections to the hippocampus, which plays an important role in learning and memory.

In a second part of the study, Dr. Halassa’s group employed a technique called optogenetics, which uses light to turn nerve cells on and off, to test whether altering TRN nerve cell firing affected attention behavior in the mice.
In one experiment, mice learned to associate a visual stimulus with food. Well-rested mice took just a second or two to find food when a stimulus was presented, while sleep-deprived mice took much longer. By turning on TRN cells that specifically controlled the visual part of the thalamus, as would happen normally in sleep, the rested mice behaved like they were sleep deprived. On the other hand, when the researchers turned off these TRN cells, sleep-deprived mice quickly found the food.
“With a flick of a light switch, we seemed able to alter the mental status of the mice, changing the speed at which information can travel in the brain,” says Dr. Halassa. Mapping brain circuits and disrupting their pathways will hopefully lead to new treatment targets for a range of neuropsychiatric disorders, he adds.

Hyper-connected neurons in "high-functioning" autistic people is information overload. The severity of social impairment means higher stress. This in turn is thought disorientation, anxiety etc. Those with autism or schizophrenia will be even more stressed if they have less sleep spindles AND are lonely - more so autistic individuals. There's a wealth of information on the forum in various threads, this thread, schizotype (correlating with the C's comments about "genes ASSOCIATED with schizophrenia") - psalehesost's post on separation/overlap & a lot more - shijing's post (#16) on the "origins of autism" thread I found interesting too,

CFS involves a large variety of symptoms (71,72), the chief ones being extreme fatigue, post-exertional malaise and/or fatigue, sleep dysfunction, muscle pain, and symptoms involving the brain that are significant but less profound than in autism (e.g. cognitive and memory difficulties).

The author proposes that these differences result at least in part from the different ages at onset. Autism develops early in life, before the brain is completely developed and before puberty, while the onset of CFS occurs after brain development is completed and (for the most part) after puberty.

Pangborn (73) has discussed five hypotheses that have been suggested to explain the higher prevalence of autism in boys. Of these, the one that appears to be most consistent with the present author’s hypothesis of a common pathogenesis between CFS and autism is the one put forward by Geier and Geier (74). Their hypothesis proposes that the higher prevalence of autism in boys results from the potentiation of mercury toxicity by testosterone, while estrogen is protective. There is increasing evidence that mercury was a significant factor in the etiology of many cases of autism, because mercury-containing thimerosol was used as a preservative in vaccines given to them. Since thimerosol was removed from childhood vaccines, the number of new cases of neurodevelopmental disorders, including autism, has been found to be dropping (75).

The present author has proposed a hypothesis (76) to explain the higher prevalence of CFS in women, involving an additional bias toward oxidative stress due to redox cycling in the metabolism of estradiol when certain polymorphisms are present.

With regard to symptoms, it seems likely that the role of methylation in the formation of myelin basic protein (77) is at least part of the explanation for the major problems in brain development in autism and the symptoms that result from them.

Fatigue is not recognized to be a major feature of autism. However, it should be noted that the evaluation of fatigue is usually based on self-report, which is not possible in children who are unable to speak. Also, it seems possible that fatigue may be manifested differently in very young children as compared with adults. Features such as hyperactivity and irritability may reflect fatigue in these patients.

Chronic pain may also be difficult to identify and characterize in children who do not have speech. A recent paper suggests that chronic pain may be the initial presenting symptom in cases of undiagnosed autism (78).

Many of the other phenomena found in CFS are also found in autism, but historically they have not received as much attention in autism as the brain-related symptoms, perhaps because the latter are so striking and profound. Some of the other phenomena that autism has in common with CFS in addition to those already mentioned are elevated proinflammatory cytokines (79), Th2 shift in the immune response (80), low natural killer cell activity (81), mitochondrial dysfunction (82, 83), carnitine deficiency (83), hypothalamus-pituitary-adrenal (HPA) axis dysfunction (84), gut problems (85), and sleep problems (86).

and also the last 6 paragraphs from "the effects of loneliness on physical and mental health" thread. Genes associated with cancer, depression, increased inflammation etc were found to have different levels of expression in the brains of lonely people. (I'm thinking more along the lines of the offspring of schizophrenic/autistic/ASD people & any effects that skip generations)

Then there's the recent signs article http://www.sott.net/article/283741-Sensory-processing-disorders-and-autism-show-structural-differences-in-brain-wiring which makes me wonder about the structure & "bridge" between autism & schizophrenia (distinction/overlap) in terms of duplicates & such (schizotype thread) where a group of shared genes added or missing means schizophrenia or autism or others like epilepsy, ADHD. (#27 schizotype thread)

As things stand though, no vaccines, a keto diet, plenty of sleep (consistent 7-ish hours unbroken should suffice) the right supplements in the right doses will go a very long way for these things. But not before TSHTF & I can only hope that after it... well who knows?