Biopsychosocial Psychiatry
Ian Goddard
The following reviews a new book by Douglas Bremner, an Emory
University psychiatrist who argues that many major psychiatric
conditions are the result of environmental stressors. Modern
psychiatry views such conditions as arising from organic brain
disorders independent of environmental psycho-social insults.
In accord with that view, psychiatric treatment has shifted
since the 60s from psychotherapy to drugs and electroshock.
Bremner's contrary view matches the argument I've made:
http://groups.google.com/groups?selm=3c69481b.48309710%40news.erols.com
http://groups.google.com/groups?selm=3c93f1d0.71349812%40news.erols.com
that a biological basis of psychiatric conditions does not
rule out psychosocial insults as possible causal mechanisms.
In short, perhaps you can be "driven crazy" by the environment
and such would manifest as distinct neurological malfunctions.
However, such malfunctions would merely be the symptoms, not
the cause. Therapeutic interventions that merely treat the
symptoms would not constitute adequate genuine treatment.
Emory University Health Sciences Center
Emory researcher claims stress-induced changes in brain can create
psychiatric disorders
Years of research come together in a book explaining how stress
affects the brain
ATLANTA -- Emory University psychiatrist J. Douglas Bremner, M.D.,
has compiled more than ten years of research, reflection, and
observations as a clinical psychiatrist in a book that explains how
stress-induced changes in the brain may account for some psychiatric
disorders, including Post-traumatic Stress Disorder (PTSD),
dissociative disorders, borderline personality disorder, adjustment
disorder, depression, and anxiety.
The book "Does Stress Damage the Brain? Understanding Trauma-Related
Disorders from a Neurological Perspective," outlines the theory that
there is a biological basis for trauma-related disorders which can
be essential in diagnosing and treating such disorders. This view of
trauma spectrum disorders, as Bremner calls them, is a departure
from the widely held view in psychiatry that psychiatric disorders
are completely different from one another, and have different
causes.
The idea of trauma spectrum disorders came out of research conducted
by Bremner and colleagues when he was a young psychiatry resident at
West Haven, VA Hospital and Yale University Hospital, During an
experience in the wee hours of the morning with a Vietnam War combat
veteran who was trapped in the middle of a post-traumatic
"flashback," Dr. Bremner was struck by the seemingly reflexive and
uncontrollable nature of the symptoms, which were similar to those
of patients having seizures. Dr. Bremner wondered if the flashbacks
represented a neurological rather than a psychological condition, as
they were considered to be at that time.
"When patients are having flashbacks, as my veteran was, they are
unaware of what is going on in the present," said Dr. Bremner.
"Patients often describe flashbacks as if a movie were playing in
front of their eyes, complete with visual images, sounds and
smells." Dr. Bremner theorized that the flashbacks could involve the
same brain areas that are affected by seizures, most importantly the
hippocampus, which is affected in 80% of epilepsy cases. Subsequent
PET (positron emission tomography) studies with trauma victims
showed a significant and direct link between a reduction in the
volume of the hippocampus and PTSD.
Bremner emphasizes in his book that all bodily functions are linked
in one way or another to the brain. In a stressful situation, the
brain automatically sends signals that release hormones, including
cortisol and adrenaline. The heart pumps faster; blood pressure goes
up; and blood flow shifts to parts of the body that need it the most
such as the brain and muscles so we can think fast and fight or run.
If the brain overcharges for a prolonged period of time in response
to stressful stimuli, the body does not have a chance to recuperate
and the results can be deadly. "If stress has effects on the brain
and neurological function, then stress has effects on all parts of
the body including the heart, blood vessels, the immune system, and
the digestive system," says Bremner. "The long list of damaging
effects can include heart disease, memory impairment, depression,
and even increased susceptibility to stroke and cancer."
"Knowledge is power." Dr. Bremner adds. "Our patients will benefit
from a greater knowledge of the potential effects of stress on mind,
body and spirit. It is essential that physicians talk to their
patients and determine what is going on in their lives before making
a diagnosis."
Dr. Bremner's background includes degrees in both psychiatry and
neuroradiology, fueled by an intense fascination with the link
between trauma and its biological effects. With the help of advanced
PET technology, Bremner and his team of Emory researchers continue
to peer into the brains of individuals with PTSD hoping to further
determine the relationship between trauma and functionality, so that
future victims can be cured. At Emory, he is director of the Center
for Positron Emission Tomography and assistant professor of
psychiatry and behavioral sciences. He also serves as director of
mental health research at the Atlanta Veterans Administration
Medical Center.
"Understanding of the human brain is more important now than ever "
said Bremner. "One thing I can say from my clinical experience is
that people in our country will be sorting out their response to the
tragic events of September 11 for many years to come. There are many
patterns of response to that tragedy that can be compared to other
traumatic events from prior history. However, in many respects this
particular event was unprecedented. The constant threat of terrorist
activity is an anomaly."
###
Media Contacts: Kathi Ovnic Baker, 404/727-9371, kob...@emory.edu
Janet Christenbury, 404/727-8599, jmc...@emory.edu
--------------------------------------------------------------------
Out-of-Body Explanation: http://iangoddard.net/paranorm.htm
Kenneth Collins
Nick Medford
<igod...@erols.mom> writes
> Modern
> psychiatry views such conditions as arising from organic brain
> disorders independent of environmental psycho-social insults.
Just out of interest, have you ever actually met a psychiatrist who
espouses this view?
I ask because I often read that modern biological psychiatry takes the
view summarised above, but have yet to meet *any* psychiatrist who
actually does take this view, despite working in a biologically-oriented
psychiatric research institute.
There is no reason at all to suppose that environmental and biological
explanations of mental illness are mutually exclusive. Indeed, it would
be bizarre to claim that they are. Equally there is no reason to suppose
that psychological and pharmacological modes of treatment are based on
mutually exclusive models. From what you say, you already realise this,
but I'm slightly baffled as to why you and many others appear to think
that nobody in psychiatry realises it.
--
Nick Medford
Kenneth Collins
In my experience, I've never encountered any Psychological or
Psychiatric profession who understands what drugs actually do within
nervous systems.
Yet the drugs are administered, in my view, 'casually', and often as
'social crutches' and 'fashion' accessories.
I did a hunger strike back in 1985.
I was 'committed'.
No Psyciatric professional would even read the [glowing] references
I'd brought with me [with foresight with respect to such
contingency].
I was treated like an 'animal' - threatened with forced medication,
being put in restraints, and permanent commettment, when all I was
doing was lying on my back, on my bed, because I was continuing my
hunger strike in the 'hospital'.
I saw all the other patients walking around like 'sombies' because
they'd been indiscrimantly-drugged.
The 'psychiatrist' assigned to me didn't even know
extremely-fundamental stuff about the Neuroanatomy [I quizzed him :-]
It wasn't until my requests to be allowed to talk to somebody who
understood Neuroscience that the Staff Neurologist did come. After
spending some time with me, he straightened things out.
Before I released, the ward I was on was completely redecorated.
I went to the Commissioner of Mental Health, seeking an Apology for
my wrongful Incarceration. It's 17 years later. I'm still waiting for
Professional Action to be taken.
So, I assert to you, if you haven't seen it, you haven't looked, or
you've a vested interest in 'covering it up'.
It needs to be Fixed, Big-Time.
There's nothing wrong with admitting it needs to be Fixed.
The only Untennable thing is to declare it all 'hunky-dory', which
only perpetuates everything that's Wrong in-there.
K. P. Collins
Nick Medford wrote in message ...
Ian Goddard
>In article <3d62f359...@news.erols.com>, Ian Goddard writes:
>>
>> Modern
>> psychiatry views such conditions as arising from organic brain
>> disorders independent of environmental psycho-social insults.
>
>Just out of interest, have you ever actually met a psychiatrist who
>espouses this view?
>
>I ask because I often read that modern biological psychiatry takes the
>view summarised above, but have yet to meet *any* psychiatrist who
>actually does take this view, despite working in a biologically-oriented
>psychiatric research institute.
IAN: Well, I can't say that I've met Harold Koplewicz,
but he's a leading proponent of bio-psychiatry and I'd
say he speaks for psychiatry's new paradigm. He said
this at the White House Conference on Mental Health:
"It's hard to believe that until 20 years ago we still
believed that inadequate parenting and bad childhood
traumas were the cause of psychiatric illnesses in
children. And in fact, even though we know better today,
that antiquated way of thinking is still out there, so
that people who wouldn't dream of blaming parents for
other types of disease, like their child's diabetes or
asthma, still embrace the notion that somehow absent
fathers, working mothers, over-permissive parents are
the cause of psychiatric illness in children. ... the
only way we can change that is through more public
awareness. I mean, essentially, these are no-fault
brain disorders. These diseases are physiological, they
respond to medicine." -- Dr. Harold Koplewicz
>There is no reason at all to suppose that environmental and biological
>explanations of mental illness are mutually exclusive. Indeed, it would
>be bizarre to claim that they are. Equally there is no reason to suppose
>that psychological and pharmacological modes of treatment are based on
>mutually exclusive models. From what you say, you already realise this,
>but I'm slightly baffled as to why you and many others appear to think
>that nobody in psychiatry realises it.
>--
>Nick Medford
Out-of-Body Explanation: http://iangoddard.net/paranorm.htm
Kenneth Collins
day, while Googling.
I couldn't believe it - my jaw hung down - it was as if I was
transported back into the Dark Ages.
It was a 'heart'-ache just to read part of it. Didn't see anything in
the Chapter from which I read that's True.
Where is Hope?
ken
Ian Goddard wrote in message <3d64408d....@news.erols.com>...
Kenneth Collins
Kenneth Collins wrote in message ...
>Yeah, I stumbled upon a similar Surgeon General's Report, the other
>day, while Googling.
>
>I couldn't believe it - my jaw hung down - it was as if I was
>transported back into the Dark Ages.
>
>It was a 'heart'-ache just to read part of it.
I RETRACT the following sentence. It's my recollection, but I
should've gone back to Verify before making such an extreme
statement. I'm not going to, so I RETRACT the following sentence.
>Didn't see anything in
>the Chapter from which I read that's True.
end of RETRACTION kpc
John H.
Good to see you back. Yes, the research is replete with examples of how
stress can exacerbate mental illness. Stress has been associated with poor
performance on testing over sustained periods or intense effort,
particularly in relation to TBI. Where it appears to cause mental illness,
do you think perhaps it has just surfaced the latent pathology?
John H.
"Nick Medford" <ni...@hermit0.demon.co.uk> wrote in message
news:us4UVDA6...@hermit0.demon.co.uk...
Kenneth Collins
Kenneth Collins wrote in message ...
>day, while Googling.
Here is the Report's URL [It seems to be associated with the Clinton
Administration.]
http://www.surgeongeneral.gov/Library/MentalHealth/
What disheartened me, on my first encounter with it, was the complete
absence of any understanding of how teaching how the 'brain'
processes information is the most-effective way of protecting folks
from environmental dynamics that, otherwise, tend to drive folks into
the "zone of randomness" [ZoR; AoK, Ap4, 5, 7, 8] unprotected, and
vulnerable.
I was also disappointed that there was no mention of the Society-wide
and International ramifications of the Same-Stuff.
Overall, my reaction to the report is that it addresses people as
"its" - 'things' to be 'operated-upon' by the 'vast armaments' of
"Mental Health" strategies.
In other words, "they're OK, and anyone at whom they point their
finger is not OK."
Which I found to be arrogant, Ignorant and "divergent" [in the sense
discussed in AoK, Ap8], rather than convergent.
There's no mention of the fact that all of 'humanity' has been 'out
to lunch' since the beginning, and the haphazard-accumulation of what
came to be accepted as 'understanding' is, itself, the main
progenitor of 'mental illness'.
The report is just another instance of Victims being further
Victimized by absence-of-understanding that deems itself 'to be
understanding'.
I want not to 'offend', but this's just more 'going through the
motions' stuff that gaains its illusion of 'efficacy' merely via
coerced consensus ["gotta buy-into this under penalty of 'failing'
grades"] perpetuated through repetition ad infinitum - they 'think'
it's 'something' because it's repeated so often within their
experience that they experience TD E/I-minimization with respect to
it, and so suffer the illusion of its 'being correct' - a classic
False Finitization [AoK, Ap4].
And what's so Exceedingly-Tragic is that the 'protests' of anyone
caught-up in the 'gears' of this Institutionalized-False-Finitization
are taken to 'constitute' "evidence" of their being 'mentally ill'.
It's the classic stacked-deck stuff of every "good ol' boy",
dues-paid, initiation-rituals-endured 'club'.
And that's all it is.
The other Exceedingly-Tragic thing is that the False-Finitization is,
supposedly, 'founded' upon all of the True-Jewels stuff produced
through the efforts of Neuroscience Experimentalists.
But it ain't - be-cause the Dictates of the 'publish or perish'
'rule' prevented anyone from doing the work of the longer-term task
of knitting-together all the True-Jewel stuff produced by the
Experimentalists.
Success was 'outlawed' by that one damn 'rule'.
And what's 'hilarious' is that, when someone endures the Ravaging
'out-cast-ed-ness' inherent in 'violating' that one 'rule', and
succeeds in the integration, the folks in the 'club' are so
'embarassed' that, even then, they can't accept the integrated thing.
I'm Sorry.
I mean not to 'offend'.
But Truth, inherent, is 'just' that Ugly.
It's 'broken', and needs to be Fixed.
Sans 'illusions' - sans False-Finitizations - with Love for Humanity,
which we Serve.
k. p. collins
>[...]
Kenneth Collins
itself, is Beautifully 'engineered' with respect to Survival within
Life-Threatening environmental circumstances.
As is discussed in AoK, Ap8, problems with respect to such derive in
the Ignorance that's prevailed with respect to such, and which
'traps' individuals within the Life-Saving dynamics, after their
necessity passes.
When such is attempted Knowingly, and Deliberately, such constitutes
the most-Shamefully-Inhumane behavior possible.
The 'ironic' thing is that it's often done, unwittingly, by
'professionals', of one form or another, asserting their
'professional' interests, disclosing that whole 'professions' are
'out-to-lunch' :-]
K. P. Collins
John H. wrote in message ...
>Mr. Medford,
>
>Good to see you back. Yes, the research is replete with examples of
how
>stress can exacerbate mental illness. Stress has been associated
with poor
>performance on testing over sustained periods or intense effort,
>particularly in relation to TBI. Where it appears to cause mental
illness,
>do you think perhaps it has just surfaced the latent pathology?
>
>
>John H.
>"Nick Medford" <ni...@hermit0.demon.co.uk> wrote in message
>news:us4UVDA6...@hermit0.demon.co.uk...
>[...]
Kenneth Collins
Ian Goddard wrote in message <3d62f359...@news.erols.com>...
>
> The following reviews a new book by Douglas Bremner, an Emory
> University psychiatrist who argues that many major psychiatric
> conditions are the result of environmental stressors.
>"When patients are having flashbacks, as my veteran was, they are
>unaware of what is going on in the present," said Dr. Bremner.
>"Patients often describe flashbacks as if a movie were playing in
>front of their eyes, complete with visual images, sounds and
>smells." Dr. Bremner theorized that the flashbacks could involve the
>same brain areas that are affected by seizures, most importantly the
>hippocampus, which is affected in 80% of epilepsy cases. Subsequent
>PET (positron emission tomography) studies with trauma victims
>showed a significant and direct link between a reduction in the
>volume of the hippocampus and PTSD.
The relatively-recent [~3 years ago] findings with respect to
hippocampal stem-cell proliferation probably indicate that such
hippocampal 'atrophy' is, at least to a degree, 'reversible'.
The 'atrophy' correlates strongly with the survival-necessity
inherent in prolonged 'stressful' environmental circumstances, and
is, itself, commensurate with TD E/I-minimization in that it would
reduce information-processing options to a relatively-small subset
that's dictated by the environmental stressors, thereby, augmenting
the information-processing 'power' that can be 'poured-into' a
relatively-narrow range of survival-pertinent behavioral
manifestations.
'Reversibility' of stress-induced hippocampal 'atrophy' would enable
post-stress-reaction return to 'normal' information-processing.
The 'catch' is that, if 'modern' psychiatric practice 'intervenes'
inappropriately, such might, itself, interfere with post-stress
hippocampal stem-cell proliferation. The 'treatment', itself,
interferes with, and 'blocks' return to 'normal'
information-processing because the 'treatment' is, itself, a
stressor - so the 'treatment' does just the opposite of it's intended
purpose.
This's all testable.
I'm not familiar with the state of the art in animal-stress
experiments, but a swim-tank design should work.
Use no blood relative subjects. All subjects same-sex.
Populate an enriched environment with 3-times the subjects that will
be subjected to the stressor [1/3 will just remain in it]
Populate an impoverished environment with the same number of
subjects.
Pre-stress, have subjects gain relatively-long-enduring familiarity
within a generously-rich experiential environment. Minimal handling,
plenty of food, lots of 'toys', exploration opportunities, exercise
equipment, etc. 'Shoot the moon' on enriching their environment.
Allow them relatively-long opportunity to become familiar with the
environment. Do not introduce new subjects after a set of subjects is
inserted into the environment [mid-test unfamiliar stuff confounds
results].
Do the stressor. 2/3 of subjects from the enriched environment
Post-stress, allow half the subjects to return to the enriched
environment with which they're familiar. [Since there're no blood
relatives, the absent 1/3 enriches the environment further.]
Remove 1/3 of the animals in the impoverished environment, and place
the other half of the stressed animals into it.
Get it? The pre- and post-experiment impoverished population has the
same number of animals, but some were replaced by stressed animals.
Allow an aclimation period of the same length as the pre-experiment
acclimation period.
Get-it? The impoverished environment is, itself, a stressor because
1. it's unfamiliar, and a large change from the familiar
pre-experiment enriched environment, and 2. because there'll be
'conflict' between the animals long-familiar with the impoverished
environment and the post-stress animals unfamiliar with the
impoverished environment.
Prediction: there'll be an observable hippocampal-rebound
differential between the subjects that're returned to the enriched
environment with which they're familiar, and the subjects that're
placed into the impoverished environment with which they're
unfamiliar. Latter-group, less-rebound.
The experimental design needs to be precise in all it's facets.
Freedom in the enriched environment. Limited opportunity, and
'obnoxious' strangers in the impoverished environment.
Tweak-it to enhance it from this "top-of-the-noggin'" description to
conform with best-practice with respect to the experimental designs
that demonstrate the hippocampal atrophy in animals.
What you've got here is an analogue for what a stressed-out human
encounters when he's virtually incarcerated in a
psychiatric-'helping' place.
Other trials might replace the impoverished environment with
excessive handling, chemical intervention, etc.
The hippocampal-rebound differential will disclose the impact of not
just enabling folks to be Free to find themselves, post-stress.
If you do this experiment, since I proposed it, you are
Ethically-bound to allow me to review your experimental design and
results [no self-fulfilling-prophecy-via-sloppy-design allowed :-]
Get in the spirit of it. Work to develop as close an analogue of a
post-stress 'hospitalization' experience as is possible.
What I'm getting at is that what has become 'deemed to be helpful'
with respect to recovery from 'stress', is actually deleterious with
respect to such recovery.
There're =many= variations of this general experimental design, all
of which will yield significant results with respect to 'helping'
environments.
The thing that makes this possible is that, animal or Human, it's all
'just' TD E/I :-]
k. p. collins
>[...]
John H.
SSRIs may well be mediated by their ability to reduce hippocampal activation
and stimulate neurogenesis in the dentate gyrus. Cortisol reduces
neurogenesis, probably via the mutual antagonism of GR occupation and nfkb
transcription; nfkb being essential not only for LTP but also neurogenesis
or probably just any any-cell-genesis. In short, the drugs, while having
their problems (I have bad reactions to SSRIs), can work remarkably well in
some people by encouraging hippocampal rehabilitation and facilitating
reactivation of the frontal cortices which tend to be quieter in depression.
It has been tested and you are wrong. Stop quoting your own ideas and have
the humility to appreciate that other people just might be right on
occasion. I am sick to death of seeing people take cheap shots. Don't insult
my intelligence with spurious ill founded propositions.
John H.
"Kenneth Collins" <k.p.c...@worldnet.att.net> wrote in message
news:Td199.25634$Ke2.1...@bgtnsc04-news.ops.worldnet.att.net...
Ian Goddard
>
>No, recent fMRI studies in Toronto demonstrated that the efficacy of the
>SSRIs may well be mediated by their ability to reduce hippocampal activation
>and stimulate neurogenesis in the dentate gyrus. Cortisol reduces
>neurogenesis, probably via the mutual antagonism of GR occupation and nfkb
>transcription; nfkb being essential not only for LTP but also neurogenesis
>or probably just any any-cell-genesis. In short, the drugs, while having
>their problems (I have bad reactions to SSRIs), can work remarkably well in
>some people by encouraging hippocampal rehabilitation and facilitating
>reactivation of the frontal cortices which tend to be quieter in depression.
IAN: Hi John! It's true that Prozac (fluoxetine) appears to
induce hippocampal neurogenesis (pubmed.com, enter 11961119).
However, Paxil (paroxetine) -- which like Prozac is a member
of the SSRI family of antidepressants -- has been shown to
cause thalamus atrophy in children treated with Paxil for
obsessive-compulsive disorder. The thalamus is of course
an important brain center. It's not clear at this time if
this is an SSRI-wide effect that might occur in all people,
but it seems reasonable to cautiously speculate that thalamic
atrophy might be an effect of SSRIs per se occurring in anyone.
About the abstracts included below....
[1] is the first study to find thalamic atrophy -- or as they
say, "decrease in thalamic volumes" -- in children on Paxil.
[2] is a follow-up that tested the hypothesis that thalamic
atrophy was a feature of OCD treatment per se, ie, perhaps
successful cognitive therapy also causes thalamic atrophy.
The results of this relatively small study indicate that
"reduction in thalamic volume after paroxetine therapy may
be specific to paroxetine treatment." With these results in
mind, I'd surely prefer a method of treatment that could be
successful and not cause atrophy of any region of the brain.
[3] is an email reply to me from one of the researchers in 1.
*****************************************************************
[1] Arch Gen Psychiatry 2000 May;57(5):449-56
Decrease in thalamic volumes of pediatric patients with obsessive-
compulsive disorder who are taking paroxetine.
Gilbert AR, Moore GJ, Keshavan MS, Paulson LA, Narula V, Mac
Master FP, Stewart CM, Rosenberg DR.
Department of Psychiatry, Wayne State University School of
Medicine, Detroit, Mich, USA.
BACKGROUND: Thalamic dysfunction has been implicated in obsessive-
compulsive disorder (OCD). While OCD frequently has its onset
during childhood, to our knowledge, no prior study has measured
neuroanatomical changes in the thalamus of patients with OCD near
the onset of illness, and before and after treatment. METHODS:
Volumetric magnetic resonance imaging studies were conducted in 21
psychotropic drug-naive children, aged 8 to 17 years, with OCD and
21 case-matched healthy comparison subjects. Magnetic resonance
imaging studies were also conducted in 10 of the 21 patients with
OCD after 12 weeks of monotherapy with the selective serotonin
reuptake inhibitor, paroxetine hydrochloride. RESULTS: Thalamic
volumes were significantly greater in treatment-naive patients
with OCD than in controls but declined significantly after
paroxetine monotherapy to levels comparable with those of
controls. Decrease in thalamic volume in patients with OCD was
associated with reduction in OCD symptom severity. CONCLUSIONS:
Our findings provide new evidence of thalamic abnormalities in
pediatric OCD and further suggest that paroxetine treatment may
be paralleled by a reduction in thalamic volume. These reductions
may, however, not be specific to paroxetine treatment and could
be due to a more general treatment response, and/or spontaneous
improvement in symptoms. Our findings are preliminary given the
small sample size and our inability to measure discrete thalamic
nuclei.
Publication Types:
Clinical Trial
PMID: 10807485 [PubMed - indexed for MEDLINE]
****************************************************************
[2] Biol Psychiatry 2000 Aug 15;48(4):294-300
Thalamic volume in pediatric obsessive-compulsive disorder
patients before and after cognitive behavioral therapy.
Rosenberg DR, Benazon NR, Gilbert A, Sullivan A, Moore GJ.
Department of Psychiatry & Behavioral Neurosciences, Wayne State
University School of Medicine, Detroit, Michigan 48201, USA.
BACKGROUND: Neurobiologic abnormalities in the thalamus have
been implicated in the pathophysiology of obsessive-compulsive
disorder. We recently reported increased thalamic volume in
treatment-naive pediatric obsessive-compulsive disorder patients
versus case-matched healthy comparison subjects that decreased
to levels comparable to control subjects after effective
paroxetine therapy. To our knowledge, no prior study has measured
neuroanatomic changes in the thalamus of obsessive-compulsive
disorder patients near illness onset before and after cognitive
behavioral therapy. METHODS: Volumetric magnetic resonance imaging
studies were conducted in 11 psychotropic drug-naive 8-17-year-old
children with obsessive-compulsive disorder before and after 12
weeks of effective cognitive behavioral therapy monotherapy (> or
=30% reduction in obsessive-compulsive disorder symptom severity).
RESULTS: No significant change in thalamic volume was observed in
obsessive-compulsive disorder patients before and after cognitive
behavioral therapy. CONCLUSIONS: Our findings suggest that
reduction in thalamic volume after paroxetine therapy may be
specific to paroxetine treatment and not the result of a general
treatment response or spontaneous improvement. These results are
preliminary in view of the small sample studied.
PMID: 10960160 [PubMed - indexed for MEDLINE]
****************************************************************
[3]
Date: Mon, 08 May 2000 23:57:13 -0400
To: Ian Goddard <xxx>
From: "Dr. Rosenberg" <xxx>
Subject: Re: Your Study
At this point it's not clear although we have several hypotheses. We
saw a differential maturation of thalamic volume in OCD patients and
controls that might reflect a neural network dysplasia with a possible
reduction in synaptic pruning in OCD pts vs controls (the normal
pruning of neural elements during peripubertal period). Cell death or
loss of cell mass is one possibility, probably best looked at in
post-mortem studies. We recently published a priority communication in
biological psychiatry (february 2000) showing decreased NAA/Cho +Cr
levels suggestive of possible neuronal dysfunction (NAA is thought to
be a marker of neuronal viability); however, more recent analysis also
suggests potential choline abnormalities. Finally, the thalamus is a
densely serotonergic region and possible aberrations in development
could lead to altered volume. This was a surprising finding, clearly
requires replication with larger samples; also, our inability to
measure subdivisions of the thalamus: we are working on a new program
that allows us to do this and we hope to delineate whether medial
regions (which we would hypothesize) would be more affected)
At 05:07 PM 5/8/00 -0400, you wrote:
>Hello Doctor Rosenberg,
>
>I just read your study in the May issue if the Archives
>of Clinical Psychiatry. I think it could prove to be a
>real breakthrough. The question I have is what's the
>cause of the observed reduction of thalamus volume?
>Could it be a result of cell death or the loss of
>cell mass? If not that, than what other cause?
>
>Thank you for your time and attention.
>
>-- Ian Goddard
>
>
"To lengthen thy life, lessen thy meals." Benjamin Franklin
Caloric Restriction: http://users.erols.com/igoddard/cr.htm
Ongoing CR-monkey-study update: "In the monkeys...those on
reduced feeding since the study started are dying at a rate
that is about half that of the monkeys receiving a full food
ration." Associated Press: Eating less may extend human life.
August 1, 2002 : http://www.msnbc.com/news/788746.asp?0si=-
Nick Medford
<igod...@erols.mom> writes
>
> IAN: Well, I can't say that I've met Harold Koplewicz,
> but he's a leading proponent of bio-psychiatry and I'd
> say he speaks for psychiatry's new paradigm. He said
> this at the White House Conference on Mental Health:
>
> "It's hard to believe that until 20 years ago we still
> believed that inadequate parenting and bad childhood
> traumas were the cause of psychiatric illnesses in
> children. And in fact, even though we know better today,
> that antiquated way of thinking is still out there, so
> that people who wouldn't dream of blaming parents for
> other types of disease, like their child's diabetes or
> asthma, still embrace the notion that somehow absent
> fathers, working mothers, over-permissive parents are
> the cause of psychiatric illness in children. ... the
> only way we can change that is through more public
> awareness. I mean, essentially, these are no-fault
> brain disorders.
>These diseases are physiological, they
> respond to medicine."
Well, of course there is some truth in that last sentence, although it would
be more accurate to say they *sometimes* respond to medicine.
I'm not completely convinced that he is actually saying environmental
causes are irrelevant, the quote seems to have more to do with the
important public-relations work of reducing stigma and blame, and it's
not clear from the above exactly which disorders he's talking about. But I
do take your point- if he's not actually saying that environment is
irrelevant, he's certainly *close* to saying it.
I still find it hard to imagine that an otherwise intelligent (one assumes)
person can think that physiology and environment have no interaction, but
perhaps it is so. I'm pleased to say that I have not come across this kind
of extreme position in UK psychiatry though.
--
Nick Medford
Nick Medford
<joh...@overhere.com.au> writes
>Mr. Medford,
>
>Good to see you back. Yes, the research is replete with examples of how
>stress can exacerbate mental illness. Stress has been associated with poor
>performance on testing over sustained periods or intense effort,
>particularly in relation to TBI. Where it appears to cause mental illness,
>do you think perhaps it has just surfaced the latent pathology?
>
I think the idea of "latent pathology" is conceptually questionable in this
context. Certainly stressors may exacerbate pre-existing tendencies, one
example would be PTSD, where it is often claimed that people do not
develop PTSD unless they had some neurotic predisposition before the
traumatic event. Personally I don't believe this is always true but it is
certainly true in some cases. But- whether it is useful or even accurate to
describe such a predisposition as "latent pathology" I'm not sure. We get
onto dangerous ground if every psychological quirk or vulnerability is
held up to be "latent pathology".
regards
--
Nick Medford
Kenneth Collins
It's a Sorrow that there's so much that's 'Dictated' by the
'whispering campaigns' that underpin 'stigmatization', when all
that's necessary is to say, "Yeah, folks disn't understand, and
errors were made."
It's not past errors that are important.
What's important is the errors impacting the Present, and the errors
that'll impact the future, if the errors of the past are not
addressed Forthrightly.
Lack of Forthrightness with respect to such actively perpetuates the
error-condition that'll inflict harm that can be prevented.
Anyway, this sort of allowing-past-errors to dictate what can be
done, 'now', is what this discussion is evoking, at least for me.
Part of it derives in the 'legalistic-lottery' predisposition of
'modern' U. S. 'society'.
Folks've come to view 'getting-rich' by sicking-lawyers on folks who
erred because they were nothing other than aligned with the
generally-prevailing ignorance in which their professions were
immersed.
And the ramifications of all that are like the 'monkey-wrench thrown
into the gears' of endeavor.
It's so Sorrow-Filled.
No one cares about anything other than 'getting-theirs' and\or
'covering their butts'.
It's part of why I openly discuss all of my 'foibles' - want to show
folks that, in reality, there's always a lot of 'stumbling-around' in
the midst of actually getting-anywhere.
But, the way things have become 'expects' everything to be devoid of
its historical basis in-error - failed-attempts, trial-and-error
experience - everyone's living in the False 'expectation' that 'all
is perfect', and any hint of 'error' is 'scandalous'.
Truth is, error is always in-there because, as is discussed in AoK,
Ap8, one cannot "see 'round the bend".
So rather than existing in the reality that the Need for Forgiveness
is built-right-in, folks 'deny' such [deny reality :-], and 'feign'
perfection.
It's 'hilarious' - it's in my everyday experience to witness folks
'saying' that NDT's stuff has been 'their view all along' - when all
one has to do to see that that hasn't been the case is to go to the
older books.
Why do I 'whine' about such?
If any one thing I've accomplished in the work I've done would've
been publicly-acknowledged, I could've given all the rest of the work
I've done - there's so much Waste in all the 'squirming'-around that
displaces simple, Forthright publication, in 'normal' ways.
Folks need to learn Forthrightness.
Folks need to learn that overcoming errors is a cause for
Celebration, not 'retribution'.
And folks need to understand that it's the absence of such that
requires one to 'jump up and down', not a spirit of 'retribution'.
If I didn't 'jump up and down', then it'd be me who'd be responsible
for the perpetuation of 'error'.
"Damned if I do. Damned if I don't."
All the Waste, inherent, needlessly exhausting energy that,
rightfully, should be going into the doing of useful Work.
I'm not 'seeking retribution'.
I'm just 'begging' folks to 'get their heads out of their butts'.
So that Neuroscience can Do what is in-Neuroscience to Do.
k. p. collins
Nick Medford wrote in message ...
Kenneth Collins
I stand on what I've posted.
That you see "cheap shots" and "insults" and "spuriousness" and
"ill-founded-ness" in-it, is your business.
I'm just working in the way I've always worked, which works, and in
which I will continue to work, because it works.
But I do find it 'interesting' that, in a thread that's stressing
"stress" in experience, and discussing the 'discord' within
biological vs.experiential-derivation of biological-modification, you
'skip' all that, and address only chemo-intervention stuff :-]
k. p. collins
John H. wrote in message ...
Peter F.
> In article <3d64408d....@news.erols.com>,
> I'm pleased to say that I have not come across this kind
> of extreme position in UK psychiatry though.
>
> --
> Nick Medford
Yours might be a case of particularly thick (thus extra desensitizing) "wool
over head". Or else you might be living on if not a different so at least a
particularly 'sheltered side' of the planet.
Yet again there are many subtly different manifestations of the
"A.E.V.A.S.I.V.E." aspect of our human phenotype.
The first post of this thread points, if not explicitly so, towards the
powerful role played by *slowly* as well as rapidly *traumatic* situations
[or some mixture of thus traumatically adverse environmental "presences"
(typically 'abusive') and/or "absences" (typically depriving)].
It also points towards existing but largely socially, medically, and
scientifically ignored terms for the insidious symptom-generating existence
of a trauma specific type of learning, and (hence not fully, or not at all,
conscious) type of memories.
These terms include PTSD, shell-shock, engrams, primal pain, '(stored)
trauma', and the acronym-concept C.U.R.S.E.S. (dots usually dispensed with).
It is not that I in any way deny the importance of varied genetic
vulnerabilities, only that what I mention above is (or represents) some of
the from our political, educational, philosophical and
scientific-anthropobiological 'scene', and our society-wide self-awareness
*most missing* aspects of "how we are", and how we got/get to be "this way"!
Peter F
--
This post of mine was, as my posts almost always are, stingily sponsored by
EAIMC Internetional Ptd. Lty., and *not just* jotted in justifiable though
author-image jeopardizing jester, but - by jove! - also with some equally
well warranted serious intent.
Peter F.
> I think the idea of "latent pathology" is conceptually questionable in
this
> context. Certainly stressors may exacerbate pre-existing tendencies, one
> example would be PTSD, where it is often claimed that people do not
> develop PTSD unless they had some neurotic predisposition before the
> traumatic event. Personally I don't believe this is always true but it is
> certainly true in some cases. But- whether it is useful or even accurate
to
> describe such a predisposition as "latent pathology" I'm not sure. We get
> onto dangerous ground if every psychological quirk or vulnerability is
> held up to be "latent pathology".
After all that fidgety, pussy-footing, postering pondering - I need *not*
ask why such 'sophistication' is one of your AEVASIVE (note that I did not
derogate by writing "neurotic") ways of *maintaining your own equilibrium*.
I bet you are mentally muddled about *your own* implicitly purported
meaning, in the above context, of the expression "neurotic predisposition"!
When you are moving in as definitionally messy a terminological territory as
this one (at and around "neurosis", PTSD, trauma, psychological pathologies,
etcetera) it is very easy to make a mess of one's own subliminally motivated
message - if ever there was one worth mentioning to start with!
I know this from first-hand experience! %->
John H.
possibilities into account because reduced stress coping can be a marker of
a number of underlying propensities (ptsd, schizophrenia, depression,
bipolar). I am not specifically thinking of genetic predispositions, there
is a range of factors associated with psychopathology eg. schizophrenia.
Recent Australian study claimed that incidence of schizophrenia correlated
with the sunlight exposure of the mother during pregnancy. This spookily is
like the MS studies indicating sunlight - vitamin D intake also showed a
correlation with MS incidence. MS is an established autoimmune disease, the
evidence for that re schizophrenia is scant though I recall articles showing
elevated autoantibodies to human hsp 70 & 60 in schizophrenia. As both of
the hsps are involved in neuroprotection immunological assaults on these
hsps suggests a dysfunction. However, as both these hsps are highly
expressed in neurodegeneration the production of antibodies to these hsps
may facilitate early identification of dying cells and accelerate
phagocytosis of the same. Given the ubiquity of hsps one wonders if the
autoimmune response to these hsps in schizophrenia is confined to the CNS.
Seems to be the case but some bacterial infections have been shown to induce
autoantibodies to hsp 60; that early viral infection - autoimmune link,
particularly in the first year of life when the infants immune system is
maturing.
A recent publication has demonstrated a remarkable link between genes and
environment.
Molecular Psychiatry
2002, Volume 7, Issue 6
Early maternal deprivation reduces the expression of BDNF and NMDA receptor
subunits in rat hippocampus
M Roceri, W Hendriks, G Racagni, B A Ellenbroek and M A Riva
Using a mouse model that recapitulates many features of schizophrenia, the
authors showed that early maternal deprivation resulted in long term
declination of BDNF and NMDA receptor subunits in the hippocampus. I find
this interesting because in a recent study
Nature Neuroscience
Published online: 6 May 2002, doi:10.1038/nn853
June 2002 Volume 5 Number 6 pp 539 - 545
A rapid switch in sympathetic neurotransmitter release properties mediated
by the p75 receptor
it was demonstrated that BDNF changed an excitatory sympathetic neuron
myocte to an inhibitory mode after 15 minutes of transfusion. This action is
mediated via p75 which allows for ceramide release and nfkb transcription.
The jury is still out but it appears that while sustained expression of
these factors can precipitate cell death the primary function is protective
and it is believed the known neuroprotective effects of tnfa are mediated
via the p75 receptor. Its a broad stretch, from myocyte to CNS but makes me
curious because some studies have indicated that in early onset childhood
schizophrenia attentional difficulties are apparent and loss of inhibitory
function may be significant here..
The loss of BDNF in the hippocampus, apart from reducing neuroprotective
mechanisms, may limit LTP creation. Mattson somewhere has demonstrated that
hippocampal LTP is dependent on nfkb transcription and while some hold the
position the hippocampal LTP is solely about memory I am inclined to the
view that it also plays an integral role in attentional matters.
Additionally, NMDA activity is supported by nfkb transcription and
Neuron, Vol. 24, 401-414, October, 1999,
Essential Role for TrkB Receptors in Hippocampus-Mediated Learning.
The hippocampus is very susceptible to stressors, I believe it contains the
highest density of glucocorticoid receptors in the human CNS. These
receptors are of two classes, MR and GR. MR is activated at low levels of
gcs and I think has a 10:1 binding preference over GR. However once gcs
reached a certain concentration gr occupation will occur and gr occupation
anatagonises nfkb transcription. MR enhances nfkb, I find it interesting
that:
Neuroendocrinology 1992 Jun;55(6):621-6 Related Articles, Books
Antidepressants increase glucocorticoid and mineralocorticoid receptor mRNA
expression in rat hippocampus in vivo.
and some other studies I've seen showing how therapeutic drugs often induce
neuroprotective functions. Eg
The Mood-Stabilizing Agents Lithium and Valproate Robustly Increase the
Levels of the Neuroprotective Protein bcl-2 in the CNS
Guang Chen, Wei-Zhang Zeng, Pei-Xiong Yuan, Li-Dong Huang, Yi-Ming Jiang,
Zhen-Hua Zhao, and Husseini K. Manji
Bcl2 is an intracellular membrane related protein that plays a critical role
in regulating cell death, it is believed some cancer cells defeat apoptosis
via increased bcl 2 expression, which has been consistently shown to provide
cellular protection.
and,
Journal of Neurochemistry 79 (1), 63-70
© International Society for Neurochemistry
Dopamine mediates striatal malonate toxicity via dopamine
transporter-dependent generation of reactive oxygen species and D2 but not
D1 receptor activation
These, together with other studies show how even the administration of
antioxidants, omega 3's(antiflammatory effect), and drugs that reduce
immunological activation can have a significant bearing on outcomes. This
contrast between mr and grs is also interesting because of a study I looked
at sometime ago that indicated mild stress for up to 6 hours enhances
cognitive function but beyond that a slight declination sets in. Sustained
significant stress may saturate mr availability leading to gr occupation and
subsequent deleterious effects. All the moreso given gr occuatpion decreases
bcl 2 expression ...
Sustained stress also disrupts pfc dopaminergic function(which may allow
hippocampal over activation, not sure), given recent findings re loss of
Darrp 32 in shizophrenia(only in dorsolateral), I wonder if the loss of
severe dopaminergic regulation is an advanced stage of the disease
particularly as this study was on deceased schizophrenics.
In that Nature 1998 article re cortisol levels and hippocampal atrophy the
researchers noted cortisol levels correlated with memory and hippocampal
atrophy. Not only via LTP neuroprotection inhibition, sustained cortisol
also reduce neurogenesis in the dentate gyrus, and the emerging concensus
now is that this region 'feeds' the hippocampus with new cells, one
researcher claiming up to 5,000 per day. Certain evolutionary sense in that
because the hippocampus is amongst the hardest working areas of the brain,
has the highest density of NMDA receptors (associated EAA and NO, both
potentially neurotoxic), and the highest gc levels. So if any area of the
human brain needs fresh cells that's it.
I can't find this article but I do remember reading how early maternal
deprivation can lead to altered cortisol response but only later in life ...
. It is as if this alteration can be hidden for quite some time. Early life
events(eg. first trimester) and diet can have a important effects on later
development
or contribute significantly to disease progression. In recent imaging
studies of early childhood onset schizophrenia however, the massive cell
loss across many regions of the CNS suggests that this much more than
something that could ever be mediated by stress or life experience;
particularly for people in their teens when the HPA axis at least tends to
have a better balance (some suggestion that with age or repeated stressors
it gradually leans the wrong way). The cell loss is substantial and rapid.
Recent news report also claimed that schizophrenics had a change in the
microglial cells leading to over activation, this seems promising because
the cell loss in shizophrenia is widespread and clearly immunological
elements are involved. This is interesting given the autoantibodies to
hsps(not in all patients) and the sunlight qtn because sunlight via vit D
generates TGFb which suppresses immunological activation.
Even mild head trauma has some association with reduced cognitive capacities
under stress and transient symptoms in the absence of any identifiable
organic abnormality. One study showed altered cortisol responses as a result
of mild head trauma and this appears to a frequent occurrence in TBI though
the cause of this remains unknown; the only hint I have seen is that even
remote trauma can affect PVN afferents thereby disrupting the HPA axis.
Environmental factors can also affect TBI outcome: eg brain injured children
from not so good families have poorer long term outcomes, the constant
stressors during the recovery period make for a poorer prognosis.
Stress impacts on most psycho pathologies. Reasons are varied and complex,
beyond me. Except in depression, where less extreme stresses induce serious
mental illness I would keep in mind the possibility of underlying
contributors; even a bad mommy.
As usual, its incredibly complicated, enough to make me insane so I'm going
back to my computer game.
John H.
"Nick Medford" <ni...@hermit0.demon.co.uk> wrote in message
news:EeS+5JAQ...@hermit0.demon.co.uk...
Kenneth Collins
We've 'tangled' in the past, interspersed with some 'hope', here and
there. What I post, here will hopefully fall into the
interspersing-of-'hope' 'portion' of out interaction.
I expect that the augmented-sunlight correlation actually 'points' to
a functional correlation that has to do with the 'stress' a Mother
endures while she's carrying her Infant.
Get it? Augmented exposure to sunlight tends to correlate either with
relative-absence of 'leisure', or relative-abundance of 'leisure',
either of which constitute 'stressors', the first, via its
'coersiveness', the latter via its tendency toward 'lack of focus'.
In both conditions, the Mother's TD E/I tends to go relatively-high,
which means that the Mother's biochemistry tends to go commensurately
'willi-nilli', which, can communicate to the fetus via shared
biochemical factors, thus, impacting fetal development.
So, I suggect that the 'sunlight correlation' needs to be explored in
terms of what it means with respect to these other factors.
Because, let's face it, if 'augmented sunlight' were, itself,
schizophrizogenic, then, back in our evolutionary roots, there'd be
only 'schizophrenics', 'cause folks were in-sunlight, abundantly.
The next thing is with respect to 'early-onset' wide-spread
cell-loss. As is discussed in AoK, Ap8, this can occur as a function
of a Child experiencing long-term "consistent inconsistency". My
studies lead me to Assert that any Child can be driven to
'schizophrenai' via experiencing of long-term "consistent
cinonsistancy".
The cell-loss derives in TD E/I-minimization, which 'blindly' and
automatically 'eliminates' any neural activation that can be
eliminated via TD E/I-minimization without resulting in TD E/I(up).
'Eliminated' neural activation correlates to cell-atrophy.
Where the "consistent inconsistency" comes in is in the way that it
'thwarts' convergence via TD E/I-minimization by
continuously-modifying the external-environmental stuff with respect
to which the TD E/I-minimization mechanisms function.
Therefore, being unable to converge upon TD E/I-minimization in any
consistent way, the 'brain' [nervous system] converges upon TD
E/I-minimization is an externally-meaningless way, gradually
'whittling' within itself massively and seemingly indiscriminantly.
This sort of thing tends, strongly, to be inter-generationally
perpetuating because a young Child's information-processing
capabilities so out-strip those of an adult who was raised within a
"consistently inconsistent" environment that the adult is
actively-induced to inflict information-processing-'leveling' 'force'
through the administering of "consistent inconsistency", even if
there's sufficient neural stuff left within the adult nervous system
to do otherwise. The 'adult' imposes the 'image' of her/his Childhood
Suffering upon her/his own Young Child, and the cycle of
externally-induced augmented neural atrophy repeats. [See "dynamic
subordinate coupling", "sensory and motor templates", "inductive
learning" in AoK, Ap5, and all of Ap8. Ap7 provides the 'antidote',
but the problem is that, before a Child can understand the
'antidote', the Child's capacity for understanding is 'stripped-away'
via coersive consistent-inconsistency.
The other thing that your post evoked is that all the low-'level'
stuff cited is 'just' the 'nuts and bolts' stuff of TD
E/I-minimization.
Note well, I'm not saying this in a 'derrogatory' way - =just= in a
way that will, hopefully, 'open the door' to folks' realizing that,
if they look for it, folks'll =always= find the unifying-stuff that's
rigorously-correlated to TD E/I-minimization [which is WDB2T], and
through which, all of the 'nuts and bolts' stuff becomes an
'edifice', rather than 'scattered'-pieces stuff.
That is, WDB2T forms the 'superstructure' that 'aligns' all of the
'nuts and bolts' stuff, so the 'nuts and bolts' stuff can be,
very-successfully, approached via WDB2T - via experimental approaches
which cross-correlate each 'nut' and each 'bolt', and their mutual
correlations, with TD E/I-minimization.
TD E/I-minimization is an =easily= observed "Rosetta Stone" that
'opens up' the whole nervous system to understanding.
The usefulness of any experiment that looks at 'nuts and bolts' stuff
can be greatly enhanced through, simultaneously, 'mapping' the 'nuts
and bolts' stuff onto TD E/I [remember the 'TD' is short-hand for all
of the Neuroanatomy - all of the neural topology].
Cheers, John,
k. p. collins
John H. wrote in message ...
Kenneth Collins
>stuff [...] is 'just' the 'nuts and bolts' stuff of TD E/I-minimization.
>
>Note well, I'm not saying this in a 'derrogatory' way - =just= in a
>way that will, hopefully, 'open the door' to folks' realizing that,
>if they look for it, folks'll =always= find the unifying-stuff that's
>through which, all of the 'nuts and bolts' stuff becomes an
>'edifice', rather than 'scattered'-pieces stuff.
>
>'nuts and bolts' stuff, so the 'nuts and bolts' stuff can be,
John H.
> Hi John.
> I expect that the augmented-sunlight correlation actually 'points' to
> a functional correlation that has to do with the 'stress' a Mother
> endures while she's carrying her Infant.
No, in the MS studies it was found that in spite of lack of sunlight some
populations have v. low MS rates. The current opinion is that such
populations have high intakes of vitamin D via fish. I agree, MS is an
immunological condition, I don't really think schizophrenia is an autoimmune
disease except in the broadest sense; which is easier for me than most
because I don't subscribe to the idea that the immune system can so clearly
delineate self from non-self.
> Get it? Augmented exposure to sunlight tends to correlate either with
> relative-absence of 'leisure', or relative-abundance of 'leisure',
> either of which constitute 'stressors', the first, via its
> 'coersiveness', the latter via its tendency toward 'lack of focus'.
> In both conditions, the Mother's TD E/I tends to go relatively-high,
> which means that the Mother's biochemistry tends to go commensurately
> 'willi-nilli', which, can communicate to the fetus via shared
> biochemical factors, thus, impacting fetal development.
Nothing to get, flawed assumption as above.
> So, I suggect that the 'sunlight correlation' needs to be explored in
> terms of what it means with respect to these other factors.
>
> Because, let's face it, if 'augmented sunlight' were, itself,
> schizophrizogenic, then, back in our evolutionary roots, there'd be
> only 'schizophrenics', 'cause folks were in-sunlight, abundantly.
You've inverted it, its lack of sunlight.
> The next thing is with respect to 'early-onset' wide-spread
> cell-loss. As is discussed in AoK, Ap8, this can occur as a function
> of a Child experiencing long-term "consistent inconsistency". My
> studies lead me to Assert that any Child can be driven to
> 'schizophrenai' via experiencing of long-term "consistent
> cinonsistancy".
If your argument is true we should all be schizophrenic because our culture
is consistently inconsistent.
> The cell-loss derives in TD E/I-minimization, which 'blindly' and
> automatically 'eliminates' any neural activation that can be
> eliminated via TD E/I-minimization without resulting in TD E/I(up).
>
> 'Eliminated' neural activation correlates to cell-atrophy.
Cell loss precedes loss of activation, cell loss precedes noticeable
cognitive decline. In depression it is overactivation of the hippocampus
that creates a problem not under activation. You are making the same logical
error so many 'pseudo Freudians' make: that mental illness is something
about aberrant information processing. Look at the range of pathologies,
neuropathologies cannot be so circumscribed, your paradigm compels you to
ignore the bleedin obvious: genetic defects(nuclear and mtDNA),
immunological insults, autoimmune responses, exogenous nasties. A model that
doesn't evolve is dead.
John. H
The difficulty of a problem is directly proportional to the coffee consumed
while thinking about it.
Peter F.
"John H." <joh...@overhere.com.au> wrote in message
news:MDYa9.17113$Cq.6...@ozemail.com.au...
One of the best (or most likely to be relevant and important)
interpretations of what this and related brain-areas of activity (1.)
'is/are doing', and (2.) how it got to be 'hyped' in the first place, is
IMO -- whilst not closing my mental doors to the possibility of
contributory and in some cases key-important: genetic predispositional
'causes', and chemical-environmental, bacterial, prionic, and viral
vandalisms --:
(1.) These readings reflects a chronic (though for obvious neurometabolic
reasons often noticably 'ebbing and flowing') "Primal Pain" (for which I
have provided a complementary definition and lavel, namely CURSES, in the
short version, and CCKHHURSES, in one of the long versions) AND its
suppression.
(2.) [I shall again mention this cause of CURSES to you the way I usually do
because nobody wants to be led by the nose to (and almost have the nose
dipped in the notion of) "selective HibernationT imploring type situations"
without getting some reward in return! The reward being the by me built-in
septic humor.]
The cause of depression (and of (from) mundanely or creatively constructive
mania and (to) completely crazy such) that we *least of all* want to
acknowledge and 'theoretically absorb' ranges from *traumatizing*
(=selective Hibernation imploring) environmental influences (or 'lived
situations') that impact so slowly and subtly and often from so early in
life as to be 'imperceptive', to the 'classical' *shell-shock*
cliché/example of fast and dramatic traumatizing experiences (or
situations).
And I shall finish-off this comment with the euphemism that you yourself
(yourselves) almost already wrote:-
It is *normally* not easy for *normal* people to focus their attention fully
enough on these major causes (SHITS come CURSES) of 'mental-motivational'
and psychosomatic "dis_eases" precisely because of how **"consistently
inconsistent our culture is"**.
If you (two) or anyone else like me to *again* post my main 'tightly
science-aligned' Web-site reference for this my position of opinionated
overview, just let me know!
> You are making the same logical
> error so many 'pseudo Freudians' make: that mental illness is something
> about aberrant information processing. Look at the range of pathologies,
> neuropathologies cannot be so circumscribed, your paradigm compels you to
> ignore the bleedin obvious: genetic defects(nuclear and mtDNA),
> immunological insults, autoimmune responses, exogenous nasties. A model
that
> doesn't evolve is dead.
Don't be so sure! Cockroaches have been around a fair while -- that's how
perfect they are! ;-)
Cheers,
Peter
Kenneth Collins
said that, if there was a prolonged 'extreme' form of experience,
then TD E/I(up) will occur, which correlates with AoK's discussion
with respect to the "zone of randomness" [Ap4], with all the
ramifications that're discussed in AoK.
I'll note, here, that in your prior post, you didn't state the
'directionality' of the sunlight correlation.
John H. wrote in message ...
>
>"Kenneth Collins" <k.p.c...@worldnet.att.net> wrote in message
>news:0kwa9.5613$p%3.42...@bgtnsc05-news.ops.worldnet.att.net...
>> Hi John.
>> I expect that the augmented-sunlight correlation actually 'points'
to
>> a functional correlation that has to do with the 'stress' a Mother
>> endures while she's carrying her Infant.
>
>No,
"no" what?
>in the MS studies it was found that in spite of lack of sunlight
some
>populations have v. low MS rates. The current opinion is that such
>populations have high intakes of vitamin D via fish.
First, I note, again, that you didn't state such in your prior post
[at least not in 'language' that say it plain].
But, beyond that, what are you, now, saying?
The nervous system is a biological system. Of course, if this or that
constituent is in a deficit-condition, such'll impact a biological
system's functioning.
The nervous system is a biological system. Ofcourse, if this or that
driving dynamic occurs in an 'extreme' form, such'll impact a
biological system's performance, and can be what underpins
'depletion' of constituents of the biological system.
It's why I ask, "'no' what?"
You're completely 'ignoring' the =fact= that the nervous system
modifies itself as a function of the stuff that drives its
activation.
>I agree, MS is an immunological condition,
I've no 'problem' with such, but in my reply to your prior post, I
was addressing 'normal' nervous system dynamics being driven by
'extreme' conditions, not immune-system function.
>don't really think schizophrenia is an autoimmune
>disease except in the broadest sense;
Again, in my reply to your prior post, I was addressing 'normal'
nervous system dynamics being driven by 'extreme' conditions, not
immune-system function.
>which is easier for me than most
>because I don't subscribe to the idea that the immune system can so
clearly
>delineate self from non-self.
I wasn't discussing immune system function.
I was discussing nervous system function.
I've discussed how, and why, nervous systems 'normally' clearly
delineate between 'self' and 'not-self'.
In my reply to your prior post, in the 'section' dealing with
'schizophrenai', among other things, I discussed how such
'delineation' can 'break-down' as a consequence of 'extreme'
experiential-environmental conditions.
>> Get it? Augmented exposure to sunlight tends to correlate either
with
>> relative-absence of 'leisure', or relative-abundance of 'leisure',
>> either of which constitute 'stressors', the first, via its
>> 'coersiveness', the latter via its tendency toward 'lack of
focus'.
>> In both conditions, the Mother's TD E/I tends to go
relatively-high,
>> which means that the Mother's biochemistry tends to go
commensurately
>> 'willi-nilli', which, can communicate to the fetus via shared
>> biochemical factors, thus, impacting fetal development.
>
>Nothing to get, flawed assumption as above.
I stand on what I posted.
>> So, I suggect that the 'sunlight correlation' needs to be explored
in
>> terms of what it means with respect to these other factors.
>>
>> Because, let's face it, if 'augmented sunlight' were, itself,
>> schizophrizogenic, then, back in our evolutionary roots, there'd
be
>> only 'schizophrenics', 'cause folks were in-sunlight, abundantly.
>
>You've inverted it, its lack of sunlight.
In your prior post, you didn't state the 'directionality' of the
sunlight correlation.
I stand on the overall position of what I've posted, which said that,
if there was a prolonged 'extreme' form of experience, then TD
E/I(up) will occur, which correlates with AoK's discussion with
respect to the "zone of randomness" [Ap4], with all the ramifications
that're discussed in AoK.
>> The next thing is with respect to 'early-onset' wide-spread
>> cell-loss. As is discussed in AoK, Ap8, this can occur as a
function
>> of a Child experiencing long-term "consistent inconsistency". My
>> studies lead me to Assert that any Child can be driven to
>> 'schizophrenai' via experiencing of long-term "consistent
>> cinonsistancy".
>
>If your argument is true we should all be schizophrenic because our
culture
>is consistently inconsistent.
Whose culture? I thought you were in Austrailia?
Anyway, within any 'culture' consistent-inconsistency is, typically,
not the 'norm' because, typically, within any interactive-group,
there's 'coersed-consensus' that's consistent to an 'extreme'. The
only 'difficulty with respect to such is, as I've discussed in recent
posts, the nervous system tends, strongly, to automatically 'blind'
itself to the coersed-consensus stuff, leaving folks subjected to it
feeling that it's just 'normal' stuff. Humanity-wide, the 'mantra'
with respect to such is "It's just human nature [don't bother trying
to change anything, it's just human nature]." [Your reply to my
response to your prior post, and your only other reply to anything
I've posted during this online 'life, exert 'force' toward some
'goal' known only to you.]
Me? "Whittle, whittle, whittle... [AoK, Ap5]
>> The cell-loss derives in TD E/I-minimization, which 'blindly' and
>> automatically 'eliminates' any neural activation that can be
>> eliminated via TD E/I-minimization without resulting in TD
E/I(up).
>>
>> 'Eliminated' neural activation correlates to cell-atrophy.
>
>Cell loss precedes loss of activation, cell loss precedes noticeable
>cognitive decline.
Do you know the meaning of "built-in redundancy"?
Nervous systems have such in large-measure, so, of course, the
built-in redundancy must be 'eliminated' before there will be
'certifiable' symptioms.
But, if one looks, one will also easily observe behavioral correlates
of the 'abnormal' cell-death long before the onset of 'certifiable'
symptoms.
And one needn't restrict one's observations to the subject. One need
just study the subject's experiential circumstances [of corse,
without 'confounding' the subject's experiential circumstances. e. g.
without the 'magic-wand' of one's presence evoking experiential
circumstances which are other than the subject's experiential
circumstances [like consistently-inconsistent stuff being,
temporarily, 'put-on-hold' because an 'observer' is present. I see,
and document, this sort of 'magic-wand' stuff routinely, which
discloses the 'ugly' reality that folks're 'aware' with respect to
the 'inappropriateness' of the consistent-inconsistency what they're
inflicting upon the 'subject'.]
>In depression it is overactivation of the hippocampus
>that creates a problem not under activation.
Are you saying that I asserted such? I did not, not only in my reply
to your prior post, but =never=.
TD E/I(up) is 'overactivation'.
Neural activation going-'random' is 'overactivation'.
>You are making the same logical
>error so many 'pseudo Freudians' make: that mental illness is
something
>about aberrant information processing. Look at the range of
pathologies,
>neuropathologies cannot be so circumscribed, your paradigm compels
you to
>ignore the bleedin obvious: genetic defects(nuclear and mtDNA),
>immunological insults, autoimmune responses, exogenous nasties.
All you're doing, John, is projecting your own 'preconceived-notions'
stuff upon 'me'.
Why?
It's known only to you.
One thing is clear, thoug, you're either not reading what I'm
posting, or you don't comprehend what I'm posting, or you've read,
comprehended, and just want to see how I'll react to a pile of B. S.
heaped-up before me, or you're just out on a [rather mean-spirited]
'lark'.
>A model that doesn't evolve is dead.
I Agree.
If it's the case that you're 'serious' about this response of yours,
get thee before a mirror, and read your statement to yourself :-]
k. p. collins
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