Testosterone and Sleep: Support for Sleep Theory

James Howard phis at sprynet.com
Thu Jan 23 17:21:09 EST 1997


Testosterone and Sleep: Support for Sleep Theory
at http://www.naples.net/~nfn03605
James Howard

In 1994, it was determined that testosterone makes obstructive sleep apnea
worse.  This is the finding of the following research from 1994.  Following this
quotation, however, one can see that it is not a simple effect of testosterone
on airway passages.

"Testosterone is thought to play a role in the pathogenesis of obstructive sleep
apnea (OSA), but the mechanism is unclear.  We present a case in which
testosterone administration induced or exacerbated OSA in a 13-year-old male.
We demonstrated that exacerbation of OSA by testosterone was associated with an
increase in upper airway collapsibility during sleep, and that this improved
after cessation of hormone administration.  Our data strongly suggest that the
mechanism by which testosterone administration may induce or exacerbate OSA is
through an influence on neuromuscular control of upper airway patency during
sleep."  (American Journal of Respiratory and Critical Care Medicine 1994; 149:
530)

This report is supported by some earlier reports.  However, some reports suggest
that testosterone replacement in hypogonadal men significantly increases "both
apneas and hypoapneas" but that this is a "highly variable event with some
subjects demonstrating large increases in apneas and hypoapneas when androgen
[testosterone] was replaced, whereas others had little change in repiration
during sleep."  This report also studied airway dimensions and concluded that
"Upper airway dimensions, on the other hand, were unaffected by testosterone.
These results suggest that testosterone contributes to sleep-disordered
breathing through mechanisms independent of anatomic changes in the upper
airway." (Journal of Applied Physiology 1986; 61: 618)

Another study of testosterone replacement in hypogondal men produced some
similar results, along with some additional information that allows me to apply
my theory of sleep and produce an explanation of the connection of testosterone
and sleep apneas.

"Obstructive sleep apnoea developed in one man and markedly worsened in another
man in association with testosterone administration. Both of these subjects also
exhibited marked decreases in oxygen saturation with the development of cardiac
dysrhythmias during sleep and large increases in haematocrit. The remaining
three hypogonadal men did not demonstrate significant sleep apnoea either on or
off testosterone. The percentage of sleep time spent in REM sleep increased from
14 +/- 3% to 22 +/- 2% when the men were receiving testosterone (P less than
0.01), but the episodes of sleep apnoea tended to occur during non-REM sleep. We
conclude that in some hypogonadal men, replacement dosages of testosterone may
affect ventilatory drives and induce or worsen obstructive sleep apnoea. The
obstructive sleep apnoea syndrome is a potential complication of
testosterone therapy."  (Clinical Endocrinology 1985; 22: 713)

Testosterone appears to produce apneas due to collapse of the airway and apneas
that occur without collapse of the airway.  I developed a theory of sleep that
may explain this apparent paradox.  (For full detail, I invite you to read my
theory of sleep at http://www.naples.net/~nfn03605 on the web.)  It is my
hypothesis that the hormone, dehydroepiandrosterone (DHEA), is necessary for
activation of the nervous system.  This has allowed me to produce a theory of
"sudden infant death syndrome," based on too little DHEA during sleep to
maintain functions of the brainstem.  When I was working on my theory of SIDS,
it became quite apparent that infants who produce too much testosterone are more
prone to SIDS.  This has allowed me to explain the connection of testosterone
with apneas in men.

My theory suggests that all genes use DHEA to function.  Testosterone causes the
genes of "testosterone target tissues" to absorb extra DHEA for their functions.
For example, this is why men have larger, more powerful muscles than women.  So,
the increased testosterone of men reduces the availability of DHEA, therefore, I
suggest sleep apneas occur more in men because of reduced availability of DHEA
for proper nervous stimulation.  According to my theory of DHEA function, all
tissues compete for DHEA.  Therefore, in a man of low DHEA, administering
testosterone as in the report above, will cause some tissues to absorb extra
DHEA and reduce already low DHEA.  This may cause either the nervous stimulation
of the airways to decline, resulting in a collapsed airway, or it may reduce the
DHEA so low that the brainstem ceases to function momentarily, as in SIDS.  This
situation would produce the apnea in which the airways do not collapse.  Of
course, the brainstem malfunction and airway collapse could occur
simultaneously.  This could explain the variability of effects of administration
of testosterone in the quotation, above.  Some of the men may be hypogonadal
because of a poorly functioning pituitary-adrenal-gonadal axis, caused by low
DHEA with low testosterone as a secondary consequence.  Some of the men may have
simply not produced much testosterone along with ample amounts of DHEA.  This
second group would represent those individuals in whom testosterone
administration had no effect on sleep at all.

I have suggested that testosterone stimulates testosterone target tissues, which
absorb extra DHEA.  This effect should stimulate some increase in the production
of DHEA.  In my theory of sleep, I suggest that REM sleep is a time when the low
levels of DHEA of night increase slightly to maintain brainstem function.
(Please read my theory of sleep in detail.)  This means that testosterone
administration during sleep should increase REM sleep; this in fact is reported
in the quotation above.  I have suggested that DHEA is necessary for nervous
system function, so I would expect apneas, caused by too low DHEA, to occur
during non-REM sleep, which is a time of the lowest levels of DHEA, according to
my theory of sleep and SIDS.  This is reported above: "...but the episodes of
sleep apnoea tended to occur during non-REM sleep."

I suggest the reason men exhibit more sleep apneas than women, and why
testosterone administration in some individuals induces sleep apneas, is due to
abnormally low DHEA during sleep.  This low DHEA can manifest itself as lack of
nervous support of the muscles of the airway, lack of support of brainstem
function, or a combination of both.
James Howard





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