SIDS, melatonin, and DHEA

James Howard phis at
Sun Aug 11 17:02:35 EST 1996

My work suggests that sudden infant death syndrome (SIDS) results from
a time during sleep when melatonin is too high and this reduces DHEA
so low that there is insufficient DHEA to maintain function in the
brainstem.  (If this interests you, you should read my theory of sleep
at on the web.)  Part of my theory
suggests melatonin increases at night, which decreases DHEA, and that
increases in DHEA during sleep cause REM sleep.  I think that
melatonin and DHEA reciprocate during the night so that sufficient
DHEA is always present to maintain function of the brainstem.  As DHEA
increases to maintain brainstem function at night, the increase in
DHEA also activates areas other than the brainstem and this causes REM

My idea that DHEA causes REM sleep was supported in 1995.  "DHEA
administration induced a significant increase in rapid eye movement
(REM) sleep, whereas all other sleep variables remained unchanged
compared with placebo condition."  American Journal of Physiology
1995; 268: E107.  

With the connection of DHEA and REM sleep in mind, consider the
following quotation concerning the reduction in REM sleep that occurs
as melatonin increases.  Keep in mind that the time of maximum SIDS is
from 2 months to six months; this is the time when melatonin starts to
really increase and reduce REM sleep.  Note that at 4 months, the
adult pattern of significant increases in non-REM sleep begins to
precede the first REM sleep.  My work suggests that this is time when
melatonin is exerting its most profound depression of DHEA, therefore,
this should be the most deadly time for infants.  (You can see my
chart of DHEA and melatonin during the human life-span in my sleep
article at my website.)  The following will make more sense if you
look at my chart and read my theory.

"Electroencephalographic studies have shown that the amount of REM
sleep changes with age.  While newborns spend almost 50% of their
sleep time in REM, the percentage of REM sleep decreases to 30% by the
age of 3 months and to 20% by the age of 6 months.  In addition,
newborns enter REM sleep soon after the initiation of sleep, but by
the age of 4 month entry into sleep assumes the adult pattern in which
a significant period of non-REM sleep precedes the onset of REM sleep.
Since reduction in the amount of REM sleep is assciated with cerebral
maturation and sicne the pineal gland has been implicated both in
cerebral development and in the organization of REM sleep, the pineal
gland may be involved in the maturation of the adult REM sleep
pattern.  Prior to the age of 3 months melatonin plasma levels are low
and the characteristic circadian rhythms of melatonin are absent.
Thereafter, melatonin secretion increases and circadian rhythmicity of
melatonin becomes apparent.  Thus, the decline in the percentage of
REM sleep coincides with the emergence of melatonin secretion
coincident with the maturation of the pineal gland."  International
Journal of Neuroscience 1992; 63: 1.

If I am correct, REM sleep should exhibit a higher activity than slow
wave sleep (SWS or non-REM sleep); I think this is due to the
possibility that DHEA is an activator of nervous function.  "During
REM sleep, brain reactivity and brain excitability thus seem to be
higher than during SWS; the reactivity thresholds are lower during REM
and a stimulation more readily evokes a cortical response during this
stage than during SWS."  Physiology & Behavior 1990; 47: 1272.  What
this means is that if melatonin rises too high and DHEA is too low,
the activity caused by DHEA during sleep in the brainstem may faulter
and cause death.  I think this is the explanation of SIDS.
James Howard

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