More on SIDS: DHEA and Testosterone

James Howard phis at sprynet.com
Thu Sep 5 10:43:44 EST 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 at
http://www.naples.net/~nfn03605 on the web.)

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.

"The data show that risk male infants fail to demonstrate an increase
in wakefulness with age and reveal a lag in the maturation of REM
sleep compared to controls and female risk infants during the critical
age for SIDS.  Significant sex differences within the first six months
of life are of particular importance because of the consistently
reported higher incidence of SIDS in males than females."
Neuropediatrics 1993; 24: 8

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.  

"In postnatal infants, there is similarity between the time course of
transient gonadal steroid secretion and the age-related incidence of
sudden infant death syndrome (SIDS). The cause of death in SIDS is
generally thought to be a ventilatory arrest, but the mechanism
responsible for such an event remains unknown. Testosterone has been
demonstrated to depress ventilatory drive and increase sleep apnea in
adult men. We tested the hypothesis that the gonadal steroid
testosterone depresses infant ventilatory drive during sleep. Three
newborn male infant primates were gonadectomized after birth.
Ventilation was observed and quantified for each animal during
completely natural unencumbered sleep by plethysmography for an
average of 16 wk. Ventilatory patterns were recorded, and ventilatory
drive was challenged with hypercapnia and hypoxia during quiet sleep
on the night before and the night after testosterone administration.
Hypercapnic ventilatory drive during sleep was significantly depressed
by an average of 33.6% on the night after compared with the night
before testosterone administration. Depression of the response to
hypercapnia after testosterone was not accompanied by any change in
resting minute ventilation measured during quiet sleep. Hypoxic
ventilatory drive, incidence of apneic events, and length of apnea
were not different after testosterone. The effects of injecting a
placebo on ventilatory patterns and drive were tested by giving the
placebo to all animals on several test weeks. Placebo injections
produced no significant change in any measured parameters. These
results support the hypothesis that testosterone depresses hypercapnic
ventilatory drive during sleep in the infant primate." 
J. Appl. Physiol. 1994; 76: 1786

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.

"When preterm male and full-term male infants were compared, no
difference was seen in the T [testosterone] peak in the first day of
life.  However, the 1-3, and 60-90 days concentrations of T were
2-fold higher in the preterm group.  ...The immediate postnatal peak
in plasma T levels persisted longer in the perterm than in the
full-term male infants." Acta Paediatr. Scand. 1982; 71: 425

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.

James Howard




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