an ALS Hypothesis - extended to all 'abnormal' neural atrophy

kenneth Collins kpaulc at earthlink.net
Tue Feb 1 22:22:50 EST 2000

at last, Joy.

a little 'story'. yesterday, i, apparently, missed the usual courtesy
call that my landlord give his tennants when our building's parking lot
is being plowed after a snowfall.

as a result, my car got plowed-in.

when i went out to survey the situation, i thought, "no problem", got
out my trusty square-blade Sears [& Roebuck] garden shovel, and removed
the compacted snow from around my car, one shovel-full at a time. took a
couple of hours, but when i was done, my parking spot, and the area of
the sidewalk upon which snow had been plowed because the snow-removal
vehicle had to work around my truck, were 'works of art'.

why this 'story'?

while i was shoveling my car out of the piled-up snow, i was also
thinking about the ALS hypothesis that i'd posted, and realized that all
that it entailed had much in common with the 'predicament' in which my
car existed.

with respect to the hypothes, too, "no problem"... 'one-shovel-full' at
a time will transform it into a 'work of art'.

it's the same, 'grinding', leave no stones unturned' 'style' with which
i do any and all work. it =always= leads to the same success,
=eventually=. all that matters is keeping-at the 'shoveling'.

dag.stenberg at helsinki.nospam.fi wrote:
> kenneth Collins <kpaulc at earthlink.net> wrote:
> > i've reformatted my prior post to make online reading easier.
> Ah, now it is all right.

i Apologize for the inconvenience. i'd detected that my comm computer
had been compromised, and so i rebuilt it. but i failed to set my news
reader correctly, leaving my posts in HTML. i noted, and fixed the
problem, when, after taking the 'time' to reformat the long prior msg,
the lines were still very-long after i posted the reformatted msg. (in
the future, if a msg appears with HTML formatting, if it is saved as a
'.HTM' file, it can, then, be read in a web browser, and 'saved' as a
text file, which will (at least in some browsers and word processors)
eliminate the HTML format characters.)

> Most points in your previous message are now clearly explained.
> I think that (descrambled) hypothesis is quite worth to read. It may be
> way off road, but at least the details and reasoning deserve thinking
> about.

yes, i agree, it surely needs more 'shoveling'-work. because i'm a
'newbie' to explication of disease processes, it was never my intention
to do anything more than to do something that would allow folks to view
the problem of ALS, Huntington's, etc., through a new 'lens'.

i've seen enough, however, to be able to say, with certainty, that the
hypothesis does, at least in some of it's parts, already advance the

> > the main thing that stimmed this 'dietary' stuff was with respect to the
> > problem represented by the 'late onset' of the disease conditions, which
> > needs explication. if, in accord with the traditional view, it actually
> > is the case that a single DNA mutation results it the entirety of the
> > disease condition(s), then why is it that the stuff of that mutation is
> > activated in such a delayed way?
> For comparison: in prion diseases, it takes times for anomalous PrP to
> develop and for deposits to accumulate.

yes, there's also stuff like the gradual absorption of toxins which
would build to a threshold at which the body cannot prevent the onset of
a disease process that's correlated to the toxin.

there was a short unsigned article in today's _New York Times_ "Science
Times" section, "Exploring Alzheimer's Early Roots" that discusses a
study by V. M. Moceri of the U. of Washington. Moceri studied long-term
correlations between Alzheimer's pathology and environmental factors,
and found strong positive correlations with respect to 'poverty'.

which is in line with the ALS, etc. hypothesis that i've been

i skimmed a strikingly-similar similar study in one of the two texts
(which were with respect to ALS) that i spent some with at the Hampshire
College Library the other day. unfortunately, in my notes, all i have
are the texts' library call numbers. and one of the refs in one of the
Medline searches i posted includes roughly-similar findings (with
respect to disease dynamics in India).

so the included-emphasis of the hypothesis i posted on the need for
detailed case histories is substantiated, as is the main emphasis on the
need for a more-generalized approach.

> > >> i relied on the discussion of ALS in Kandel, et. al. for my
> > >> start. the factors that i found significant are as follows.
> > >> the Hypothesis:
> I had not earlier been able to find this among the over-long lines.

my fault, as explained at the top of this post. i apologize for the
unnecessary difficulty my failure imposed upon you.

> > >> the demyelination results from a specific brain stem lesion,
> > >> of a type analogous to the chemically-induced vestibular
> > >> lesion, or a stroke-induced lesion.
> > >> ...
> I do not see any explanation for the fact that brain stem symptoms are
> usually later in appearance than limb involvement. It also seems to
> neglect observable peripheral pathology.

it's in the hypothesis that the percipitation 'lesion' acts through the
modification of 'normal' integrated dynamics. in the example offered
with the hypothesis, a lesion alters the information-processing of the
cerebellum (which, in NDT, is a powerful 'passive', globally-acting, TD
E/I-minimization mechanism; see AoK, Ap5).

one must put-things-together. the lesion alters cerebellar function,
which results in abnormal motor-system dynamics, because, the
interminable TD E/I(up) condition that the lesion interjects prevents
normal achievment of 'type II synchronization" (as evidences in ALS
fasciculations and fibrilations.

the late onset of respiratory functionality would, therefor, be
correlated with the 'time' at which the motor-neuron's 'struggle' with
long-enduring TD E/I(up) was coming to a close, because, up until that
'time', the lesion-cerebellum couple still has feedback from the
out-of-sync motor-neuron activity with which to deal.

in this view, the onset of the respiratory dysfunction results from a
further =release= phenomenon that occurs when the motor feedback becomes
so weak that its functionality within the global TD E/I-minimization
dynamics falls below a threshold (determined by brain-stem neural
architecture) at which the brain stem areas correlated with respiration
gain precedence within the ongoing activation 'state' (i took notes on
all of the underlying nuclear groups while reading the other night. msg
back if you want specific details. but be quick. i'm being 'forced', by
my financial circumstances, to go offline.)

in other words, the demise of the motor neurons results in an =actual=
're-engineering of the neural topology of the brain stem, and, as a
result, the relationship between the respiratory nucs of the brain stem
with respect to TD E/I-minimization becomes rewired, and what remains of
the supersystem 'blindly' 'seeks-out', and 'attacks' the 'normal'
respiratory functionality as a TD E/I(up)-condition, which results in
the aberrant 'shutting-down of respiratory functionality.

it's important to be aware that, in the above dynamics, the supersystem
is 'just' 'striving', in 'normal' ways, to achieve TD E/I(min). it's
be-cause the lesioned tissue interjects 'perpetually-random',
non-minimizable activation into the TD E/I-minimization dynamics that
the 'normal' TD E/I-minimization dynamics generate the hyper-stressing
'struggle' to achieve type II synchronization back upon the motor
neurons, which constitutes an 'excito-toxic' condition with respect to
the motor neurons' metabolic functioning, which kills them, resulting in
the =obvious= disease observables that have been focussed upon, while
the more-subtle, more-globally-occurring, and much-more-significant
disease-generating stuff had gone unrecognized.

[it's off-topic, but =all= psychological & cognitive dysfunction bears
these sames 'signs', albeit, to a very-much-more subtle degree. what
happens in these psychological dysfunctions is that interminable TD
E/I(up) that's interjected from the experiential environment drives the
'normal' TD E/I-minimization dynamics in aberrant ways, with much the
same results (that is, with physically-real neural atrophic
consequences) as are described in this hypothesis. it's a =CERTAINTY=
that such more-subtle stuff enters into the onsets of what have been
considered to be 'totally-organic' diseases such as Alzheimer's, ALS,
Huntington's, etc. the discussion of these more-subtle, but nevertheless
highly-significant, considerations (which i''ve been addressing, all
along, via a trying-to-be-Gentle 'baby-talk' 'style', so as not to
'panic' folks, goes on-and-on within NDT. it's one of the things i'm
talking about when i say that "there's not sufficient 'time' left in my
Life to discuss everything that was long-ago reified, even if such
discussion is all i do with the rest of my Life. hence, my Sorrow, with
respect to the fact that no one will meet with me, in-person, to discuss
the core of such stuff.]

> > >> there are other attractive rationales for this sort of
> > >> hypothesis. the problem of the 35+ years typical onset of
> > >> ALS has to be explained. if there's a genetic flaw, then how
> > >> is it that it shows itself only after 35+ years? what's the
> > >> 'switch' that changes fully-functional motor neurons to
> > >> dysfunctional 'motor' neurons?
> Interesting question, no doubt.
> > if this sort of thing occurs, then the disease is treatable through
> > methods that eliminate the functionality of the newly-triggered stuff,
> ...
> How would you diagnose the disease 35+ years before outbreak?

=iff= there's anything to the hypothesis that i've been discussing,
contemporary 'scanning' methods would disclose the aberrant TD
E/I-minimization 'struggle', through which, what has been considered to
be the disease condition, is generated (precipitated). and sensitive
versions of those scanning methods should be able disclose the TD
E/I(up)-generating 'lesion' location. of course, all such work can only
occur with respect to deviations from a background database that tracks
'normal' (average) activation 'states'. building this
background-comparison database would, itself, be a major undertaking,
but would definitely, itself, become o font of useful insight.

> > at any rate, an explanation for the observed delayed onsets of
> > Alzheimer's, ALS and Huntington's is necessary, and it will probably be
> > the case that, when such delayed onset is explained, treatment
> > strategies will become apparent within such explanation. so explication
> > of the delayed onset is an important problem.
> > >> the one criterion that =must= be met in order to explore
> > >> this hypothesis further is, since the ocular motor system is
> > >> not affected in ALS, to culture examples of ocular motor
> > >> neurons  along with examples of upper and lower motor
> > >> neurons, and look for differences that would allow the
> > >> ocular motor neurons to survive while the upper/lower motor
> > >> neurons would not survive.
> This seems to me a profitable approach. Objections, anyone?
> > i repeat, i'm taking this position in this hypothesis because all of the
> > so-called 'indicators' that i've read of can result from excitotoxic
> > activation, which means that it's possible that the 'indicators' are
> > nothing of the kind, but 'only' by-products of a
> > more-globally-correlated set of dynamics, such as those that i've been
> > discussing in this hypothesis.
> Logical. Not necessarily true, but logical.

it's an hypothesis, done to 'goose' folks' 'wondering', and, hopefully,
their experimental explorations. by now, i've gone over the stuff of the
hypothesis sufficiently to be able to say, with certainty, that at least
some portions of it will withstand all tests.

so, in it, i've kept my word about advancing the Science.

> > anyway, that's my contribution(?) to the efforts to extinguish these
> > diseases. i could do more, but despite the fact that i've done this
> > stuff at my own expense, i've only been 'ridiculed' for having tried
> I think this (descrambled) hypothesis is quite worth to read. It may be
> way off road, but at least the details and reasoning deserve thinking
> about.

Thank you, Sir. i, again, Apologize. i'd not realized that it was my
=inadvertant= posting in HTML that had interjected 'TD E/I(up)' into our

k. p. collins

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