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Breast feeding and Sudden Infant Death Syndrome

k p Collins kpaulc at [----------]earthlink.net
Mon Jan 12 21:31:13 EST 2004

I cannot comment upon your hypothesis, but comment,
in a general way, below.

"James Michael Howard" <jmhoward at arkansas.net> wrote in message
news:2qa500d12t8fjh6s4mrbrgv85jmntsbu60 at 4ax.com...
> Breast Feeding and Sudden Infant Death Syndrome:
> Prolactin, DHEA, Melatonin and SIDS
> Copyright 2003, James Michael Howard, Fayetteville, Arkansas, U.S.A.
> This is a response to: Archives of Disease in Childhood 2004;89:22-25
> "Comparison of evoked arousability in breast and formula fed infants"
which I
> sent to the journal.  Here are the "Results" and "Conclusions" from the
> and my response.  I thought the readers here may be interested.
> "Results: Arousal thresholds were not different between breast fed and
> fed infants in QS. However, in AS breast fed infants were significantly
> arousable than formula fed infants at 2-3 months of age. There was no
> between groups of infants when sleep period length was compared at any
> Conclusions: Breast fed infants are more easily aroused from AS at 2-3
months of
> age than formula fed infants. This age coincides with the peak incidence
> SIDS."
> It is my hypothesis (1985) that the sleep-consciousness cycle is
controlled by
> interactions of melatonin and DHEA.  (It has been demonstrated that DHEA
> involved in melatonin production and melatonin is involved in DHEA
> Basically, when melatonin is high, sleep occurs, when DHEA is high,
> consciousness occurs.  As is well known, quiet sleep alternates with
> sleep.  I suggest this cycling is designed to maintain sufficient levels
> during sleep to maintain brainstem function during times of sufficiently
> DHEA that allow sleep.  When DHEA is very low, quiet sleep occurs, when
> higher, during sleep, active sleep occurs.  Prolactin is known to
stimulate DHEA
> production.  The cycling of quiet sleep and active sleep involves the
> of prolactin by melatonin with prolactin rebounding in response to levels
> melatonin.  The first sleep is the deepest, I suggest, due to the high
levels of
> melatonin at this time.  As prolactin rebounds, DHEA is produced which
begins to
> decrease levels of melatonin as sleep progresses.  This gradual reduction
> melatonin and increase in prolactin eventually reaches a level of DHEA
> induces consciousness and stops release of melatonin until DHEA production
> decreases near nighttime and begins the cycle again.  The connection
> melatonin and DHEA is prolactin.
> Breast milk contains prolactin.  I suggest prolactin occurs in breast milk
> stimulate DHEA.  Therefore, prolactin in breast milk would activate DHEA
> production, but not sufficient to induce arousal.  This would combine with
> infant's DHEA to increase DHEA during active sleep.  It is my hypothesis
> sudden infant death syndrome results from insufficient DHEA during quiet
> to maintain brainstem function.  I suggest the evolutionary value of
> in breast milk is decreased SIDS.
> [...]

If it's as you describe above - that there's a DHEA waxing
and waining that's ongoing during sleep, that indicates that
DHEA 'mediates' within more-fundamental dynamics, and
is a 'tool' within a larger set of dynamics, and not the deter-
mining thing [not the globally-integrated thing].

For those who have AoK, see Ap9 - "functional multiplexing".

If it's as James says, with respect to DHEA, then this is a case

The type of dynamics James has described are correlated, in-
general, with "ratcheting" as it is discussed in AoK, Ap5, both
with respect to hippocampal function, but in the case that
James has discussed, more-directly to the substantia nigra's
"ratchet-pawling" role with respect to the basal ganglia.

This's interesting to me because, if it's as James has described,
James has presented a 'picture' of dynamics that are correlated
to [that are in] the cross-correlation of a 'day's information-intake
with all of pre-existing memory [in NDT: "experiential total"; AoK,
Ap7 & 8].

That is, if it's as James describes, then the dynamics he has
discussed play a role in the setting of "supersystem configurations"
[AoK, Ap5] through which the new-memore cross-correlation
with old-memory occurs in a way that 'walks' "experiential
total", hierarchically.

What I've discussed, here, is relatively-easy to test through
experimental methodologies that cross-correlate manipulations
of the dynamics James has discussed [in animals, of course]
with post-manipulation behavioral manifestations.

The post-intervention stuff to look for will be the animals'
manifesting behaviors that are 'mixed-up' with respect to
the animals' prior experience [so, to be able to observe
this 'being behaviorally 'mixed-up', the test animals' behavior
must be archived to a robust criterion =prior= to inter-
vention - this can be accomplished via recording video logs
of the subjects' behaviors, say, with respect to a regime
in which the subjects are trained in mazes of augmenting
complexity, but which have, embedded within them, sub-
regions that replicate elements of the less-complex mazes
in which the animals were trained earlier. The overall goal
is to measure cross-correlation of these old learning dyn-
amics with the new demands of the increasingly-complex

If the dynamics James has discussed are as I've discussed
in this post, when intervention occurs, the animals will
manifest observable 'mix-ups' - they will exhibit a deficit
with respect to long-term =integration= - they will do
stuff that's obviously 'inappropriate' withrespect to that
which they've been observed to have formerly learned.

The experiment is 'demanding' only in that it requires
subtle evaluation on the parts of the experimenters. That
is, the video must be quantified rigorously to transcend
subjective bias.

[With respect to James' hypothesis, SIDS would occur as
a result of "supersystem configuration" dynamics having
become 'imbalanced'. For instance, back before NDT's
stuff imploded to unity, I'd routinely work beyond the 'levels'
of my own endurance. Then I'd collapse into 'sleep', but
routinely awaken 'terror'-stricken, heart-pounding like it
was going to jump out of my chest, gasping for breath -
be-cause I'd stopped breathing, What had happened was
that I'd crammed more info in-there than there was pre-
viously-accumulated transmitters, and the "supersystem
configuration" dynamics ran-into this imbalance of there
being more work to accomplish than there were neuro-
chemical 'tools' with which to carry it out - one 'part' of
the dynamics was just taking care of business, but another
'part' of them 'ran-out-of-gas' - probably because the one
'part' depleted the resources of the other 'part' - so the
overall dynamics 'failed', catastrophically. And, fortunately,
for me, this 'imbalance' broke-through to waking-conscious-
ness be-cause of its inherent extremely-high TD E/I.

Seeing all of this tonight, while considering the stuff of James'
post, causes me to 'wonder' about the pre-SIDS experience
of Infants - was their experience during that 'period' overly-
'rich'? Had they taken-in too much information, and succumb
to the 'imbalanced' "supersystem configuration" dynamics
that I routinely experienced when I was pushing myself to
integrate the information that I was cramming into the ol'
noggin' lab?

Such stuff can take the form of an Infant's Learning with
respect to a Parent's 'frazzled', overly-'caring', etc., be-
havior - "information overload" [As I've discussed in
long-former posts, newborn Infants are the most-intelligent
Beings on the face of the planet. Their Learning is proceding
=explosively=. So, if there's too much 'environmental' info
crammed-in-there, on top of this =normal= explosive
learning, the infants are subjected to stuff that's analogous
to my 'info-cramming' correlates, but, unprepared, they

The above can be researched by evaluating pre-SIDS

[Side note: It's all so interesting. My analysis of these
horrifying sleeping->waking consciousness transitions
fed right back into the ongoing convergence upon the
reification of "supersystem configuration". ["Never waste
data!" :-]]

k. p. collins

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