Biopsychosocial Psychiatry

[Kenneth Collins]

Hi John.

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 ...
>Not "every psychological quirk" but enough that we should take such
>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" <nick at hermit0.demon.co.uk> wrote in message
>news:EeS+5JAQoRZ9EwVM at hermit0.demon.co.uk...
>> In article <k7_89.15199$Cq.610323 at ozemail.com.au>, John H.
>> <johnhkm at 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
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