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ELECTRONIC ARTICLE:
Claudia M. Gerard, Kathleen A. Harris, and Bradley T. Thach
Spontaneous Arousals in Supine Infants While Swaddled and Unswaddled During Rapid Eye Movement and Quiet Sleep
Pediatrics 2002; 110: e70 [Abstract] [Full text] [PDF]
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[Read P3R] The Findings of Gerard, et al., May be Explained by Melatonin and DHEA
James M. Howard   (4 December 2002)

The Findings of Gerard, et al., May be Explained by Melatonin and DHEA 4 December 2002
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James M. Howard,
Biologist

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Re: The Findings of Gerard, et al., May be Explained by Melatonin and DHEA

jmhoward{at}arkansas.net James M. Howard

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