There is a theory about that Diane. I don't know if it has been proven but basically this guys 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. Part of the theory suggests melatonin increases at night, which decreases DHEA, and that increases in DHEA during sleep cause REM sleep. 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 sleep. If his theory is correct then he says that REM sleep should exhibit a higher activity than slow wave sleep (SWS or non-REM sleep) and 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." 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. Therefore this theorist (James michael Howard) thinks this is the explanation for SIDS. You can read more at: www.naples.net/~nfn03605/