The findings of Gerard, et al., may be explained by my sleep
mechanism,* dependent upon an interaction of melatonin and
dehydroepiandrosterone (DHEA). A recent study reported that “nocturnal
urinary melatonin excretion was significantly greater in the TC [tight
clothing] group.” (Int J Biometeorol 2002 Dec;47(1):1-5). I suggest
swaddling may increase melatonin production in babies. It is my
hypothesis that melatonin interacts with DHEA in a “melatonin – DHEA
cycle” which determines the circadian rhythm, that is, sleep and
consciousness. Very briefly this mechanism is as follows: In daytime
concentrations, DHEA is the molecule of consciousness, i.e., activation of
the nervous system. Part of this activation of the nervous system
inhibits release of melatonin (MLT) from the pineal gland. As DHEA
production declines during the day, inhibition of melatonin declines until
melatonin is released as a large bolus. Melatonin inhibits prolactin
release which stimulates DHEA production. This first, large release of
MLT, therefore, inhibits the production of prolactin and then DHEA. This
first combination of very high levels of MLT and decreased DHEA results in
the first, deep sleep, slow-wave sleep or QS (quiet sleep, Gerard, et
al.). This is the deepest sleep. It is part of my explanation of sleep
that a certain amount of DHEA is necessary to maintain the brainstem.
This is maintained by the MLT – DHEA cycle during sleep; the levels of
DHEA during this time are very low because of increased MLT of sleep. As
MLT declines during sleep, each of these cycles allows prolactin
production and increases DHEA slightly. Therefore, as sleep progresses,
sleep becomes more shallow until sufficient DHEA is produced to, again,
inhibit total MLT release from the pineal gland. Consciousness reoccurs.
It is my hypothesis that the periodic increases in DHEA during sleep
produce dreams (REM sleep) and increase as sleep wanes. (These slight
increases slightly stimulate the cortex but do not produce consciousness.)
This mechanism may be used to explain the findings of Gerard, et al., as
well as SIDS.
In the “Discussion,” Gerard, et al., point out that “Women who
traditionally swaddle their infants report that their infants would not
sleep if they were not swaddled. It is unclear what effect swaddling
exerts on infants, but it does seem that swaddling an infant results in
‘better sleep’ than leaving the infant unswaddled, as this study
suggests.” If swaddling increases melatonin, like tight clothing does in
Mori, et al., then swaddling should increase release of melatonin, which
is known to induce “better sleep.” I have suggested for many years that
it is low DHEA during sleep that results in loss of brainstem function
that results SIDS. Gerard, et al., point out that “Epidemiologic studies
suggest that swaddled and supine sleeping infants have a significantly
lower risk for SIDS than unswaddled supine sleeping infants. However,
epidemiologic studies clearly show that swaddling decreases the risk for
SIDS more than supine sleeping alone.” Melatonin concentrations in SIDS
are low (Forensic Sci Int 1990 Mar;45(1-2):171-80) and in infants with
life-threatening events (Dev Med Child Neurol 2000 Jul;42(7):487-91). I
suggest SIDS may result from a decline of the “MLT – DHEA cycle” which
reduces sufficient DHEA during sleep to support brainstem function.
Swaddling increases this cycle and protects from SIDS.
According to my explanation of sleep, if brainstem function is
decreased below a certain limit, DHEA is recruited via the catecholamines
to induce “rebound” increases in DHEA sufficient to maintain brainstem
function and often results in such levels of DHEA that consciousness is
approached or occurs. I think this is the mechanism which occurs during
awakenings from apnea and may be lacking during SIDS. This is supported
by Gerard, et al., “We found that infants have more startles in REM sleep
when unswaddled than when swaddled.” That is, if swaddling increases MLT,
then this continues the MLT – DHEA cycle which maintains brainstem
function. Also: “In any case, full arousals were shorter in duration when
swaddled than unswaddled, which resulted in the infant’s returning to
sleep more rapidly.” This indicates that background DHEA is sufficient to
maintain brainstem function which allows sleep, as opposed to insufficient
DHEA which may cause increased arousal “rebound” to sustain the brainstem.
This would explain why swaddled infants had shorter arousal durations.
(* My sleep mechanism remains unchanged from 1985. (“A Theory of the
Control of the Ontogeny and Phylogeny of Homo sapiens by the Interaction
of Dehydroepiandrosterone and the Amygdala,” Copyright 1985, James Michael
Howard, Fayetteville, Arkansas, U.S.A., Registration No. Txu 220 580)
This is available at: http://www.naples.net/~nfn03605/dheaslee.htm
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