Copyrightã 1996 James Michael Howard.
The following is a compilation of three postings to newsgroups at different times regarding my idea about Sudden Infant Death Syndrome (SIDS).
Part I (August 11, 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. 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 sleep.
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.
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 falter and cause death. I think this is the explanation of SIDS.
Part II (September 5, 1996)
Earlier, I posted my hypothesis that SIDS occurs during a time when melatonin is high and DHEA is low. I suggested that DHEA is a stimulator of the nervous system, that melatonin reduces DHEA during sleep, and levels of DHEA that are too low will result in loss of DHEA stimulation of the brainstem. Hence, when DHEA is too low, death occurs. I want to extend this with further supporting evidence that involves epidemiological findings in SIDS.
The first place to look, given my hypothesis, is the adrenal glands, the site of DHEA production. Well, I did and the adrenal glands are normal in SIDS. "Our data revealed a normal maturation of the adrenal glands in SIDS cases." (Int. J. Legal Med. 1994; 106: 224.) I decided to look elsewhere, i.e., I decided to look at the influence of testosterone on the incidence of SIDS. More boys than girls are affected by SIDS. Additionally, I have already shown that testosterone has a negative effect in HIV infection and AIDS, so this is a logical thing, for me, to check. This ...is... where the answer lies. (You may find my hypothesis of AIDS on the index page.)
If you read my first posting on SIDS, you will remember the connection of REM sleep and DHEA. The idea is that REM sleep is a healthy sign for infants during the time of SIDS incidence. (Proper amounts of REM sleep mean proper amounts of DHEA during this time.) In the following quotation, note that there is a "lag in the maturation of REM sleep" in SIDS. This indicates to me that DHEA is in low amounts as melatonin increases in the first months of life.
My idea, in SIDS and in AIDS, is that the hormone, testosterone, directs DHEA to use by "testosterone target tissues." You see, my principle hypothesis is that DHEA is required for optimal transcription and replication of DNA. Therefore, testosterone increases use of DHEA for its target tissues; they grow bigger because of this, and this is why men are bigger than girls. Men produce more testosterone. However, in a situation of limited DHEA, this can be a problem, because testosterone redirects DHEA for its target tissues. (This is why men of high testosterone to DHEA become bald.) I think the same thing occurs in SIDS. One of the main causes of SIDS, then, is a high ratio of testosterone to DHEA. The idea that testosterone is involved in SIDS has been tested in an infant primate.
Does increased testosterone cause increased SIDS in humans?
Well, I think the case is supported for male vs. female SIDS victims. SIDS is higher in "preterm" infants: "Although only 9% of infants are born at less than 36 weeks' gestation, 20% of SIDS victims are former premature infants." [Clin Pediatr (Phila) 1995; 34: 410.] Testosterone is increased in preterm infants during the time when SIDS occurs at increased frequency.
SIDS is increased in women who smoke. I have developed a theory that suggests that the rise in testosterone of puberty triggers smoking. (You can use my name and "smoking" to find this with Dejanews.) Since I think testosterone is rising in this society, I explain the increase in smoking in young people as a result of the increase in testosterone. Women who smoke, therefore, may be women of higher testosterone. While the following investigator gives credit to "sociological factors" in addition to testosterone in adolescent smoking in (Addict. Behav. 1992; 17: 459), his first publication concerning adolescent smoking and testosterone is more to the point for this treatise. "Social and psychological variables are used to explain why young people become cigarette smokers, whereas biological factors have been virtually ignored as possible determinants of that behavior. In this study, salivary testosterone was positively associated with cigarette smoking among 201 subjects 12-14 years of age. This finding suggests that testosterone should be included in future considerations of adolescent cigarette smoking." (J. Behav. Med. 1989; 12: 425.) I think the connection of smoking and SIDS is that women who smoke are higher in testosterone. They produce children who are higher in testosterone, which increases SIDS.
If testosterone is redirecting DHEA use, where is it going?
I think the DHEA is being redirected to brain structures that are testosterone target tissues. Consider that "The Nv [volume of hypoglossal nucleus - cells per mm3] of synapses did not differ significantly between SIDS cases and controls, although the total number of synapses was greater (61%) in SIDS." (J. Neuropathol. Exp. Neurol. 1995; 54: 627.) In some songbirds, testosterone has an effect on the hypoglossal nucleus. "We find anatomical correlates for each of these attributes in the nXIIts [hypoglossal nucleus]. This nucleus is 83% larger in males than in females." (J. Comp. Neurol. 1991; 307: 65.) Earlier, this reference says "Its [the hypoglossal nucleus] neurons concentrate androgens." This means that the hypoglossal nucleus is a "testosterone target tissue."
An increase in synaptic growth in lower brain structures may cause two phenomena. Firstly, it may make these structures more "mature" in that they grow faster. This could result in shorter gestation, i.e., preterm delivery. The neonate participates in the time of delivery. These neonates would be smaller, because less time would be available for growth. "Mothers of SIDS infants give birth to smaller babies in general. SIDS infants weighed, on average 85 g less at birth than their siblings and 164 g less compared with babies in nonaffected sibships. When birth weights were standardized for gestational age, most of the weight difference between SIDS infants and siblings was due to a shorter gestational age of SIDS infants, while the difference between surviving siblings of SIDS infants and births from nonaffected sibships remained. All births in sibships with a SIDS infant were intrauterine growth retarded. This may reflect factors that contribute to SIDS risk (such as maternal smoking)." (Am. J. Epidemiol. 1995; 142: 84.)
Structures in the brainstem that have excess synapses may require more DHEA in order to maintain sufficient activity of these structures. When melatonin reduces DHEA at night, there may be insufficient DHEA to properly activate these structures. The hypoglossal nucleus is in the brainstem.
SIDS should be more prevalent in women who are higher in testosterone.
Part III (September 12, 1996)
African women produce more testosterone than white women. This is very difficult to find in current journals. I know of one group of endocrinologists who measured testosterone in African American women and European American women and found much higher levels of testosterone in the African Americans, but did, or would not, publish. The following is the best I could find.
Dada ,O.A., et al., "17 Beta-estradiol, Protesterone and Testosterone in the Normal Menstrual Cycle of Nigerians," (Int J Gynaecol Obstet 1984; 22: 151)
This corresponds with the findings that testosterone is higher in black men, medium in Asian men, and lowest in white men. See Table II, page 888 in Lancet 1992; 339: 887-889. In a group of college men in the U.S., black men produce significantly more testosterone than white men (Journal of the National Cancer Institute 1986; 76: 45).
If I am correct that SIDS, and premature delivery, occur more in women with high testosterone, we should find this in black women. The following three quotations support this. (I could not find an author for the first, but it was found in PubMed.)
. . . "Variations in the Incidence of Sudden Infant Death Syndrome (SIDS), United States, 1980-1988," (Stat Bull Metrop Insur Co 1993; 74: 10)
Denmead, D.T., et al., "Placental Pathology is Not Predictive for Sudden Infant Death Syndrome (SIDS,)" (Am J Perinatol 1987; 4: 308)
Shiono, P.H. and M.A. Klebanoff, "Ethnic Differences in Preterm and Very Preterm Delivery," (Am J Public Health 1986; 76: 1317)