Biopsychosocial Psychiatry CORRECTION

Kenneth Collins k.p.collins at worldnet.att.net
Mon Aug 26 18:17:10 EST 2002


CORRECTION color

Kenneth Collins wrote in message <0kwa9.5613$p%3.429909 at bgtnsc05-news.ops.worldnet.att.net>...
>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' [molecular]
>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
>rigorously-correlated to TD E/I-minimization [which is WDB2T ^ -1], and
>through which, all of the 'nuts and bolts' stuff becomes an
>'edifice', rather than 'scattered'-pieces stuff.
>
>That is, WDB2T ^ -1 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 ^ -1 - 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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