Androgenic Hormones and Bacterial and Viral Infections

James Howard jmhoward at sprynet.com
Sat Jan 9 09:39:56 EST 1999


More on DHEA, Testosterone and Infections

James Michael Howard
Fayetteville, Arkansas, U.S.A.

I have posted here, and elsewhere, regarding my hypothesis that proper
amounts of the hormone, DHEA, are necessary for immune defense against
viruses, specifically the HIV.  One may read this in my article concerning
AIDS at my webpage, http://www.naples.net/~nfn03605/, or at my recent post,
possibly here, entitled: “Why the HIV is so Prevalent in Africa.”  It is
also my hypothesis that sufficient DHEA is necessary for immune defense
against bacteria.  (This is within my article on AIDS at the webpage.)  I
just recently found the following quotation (at the end of this post) which
directly supports my hypothesis regarding DHEA and bacteria and also
supports my ideas concerning the influence of testosterone in infections.
That is, my post regarding the HIV in Africa deals with the inhibitory
effect of testosterone on DHEA enhancement of the immune system. The
quotation, which I just found and which caused me to write this post, deals
with the inhibitory effects of testosterone on the immune system, and it
includes the conclusion: “The finding that DHEA markedly improves the
depressed immune functions and survival of animals subjected to subsequent
sepsis suggests that short-term treatment with DHEA after trauma-hemorrhage
is a safe and novel approach for preventing immunodepression and for
decreasing the mortality rate due to subsequent sepsis.”

February 11, 1996, page 3F, my “letter to the editor” of “The Morning News
of Northwest Arkansas” included the following which includes my explanation
of the connection of DHEA and testosterone in infections.  (I omitted the
introductory material and the conclusion.)

“The Jan. 17 article reported that a lot of the increase in bacterial
infections may be due to ‘antibiotic resistance.’  Healthy people are
exposed to infectious bacteria constantly, including antibiotic resistant
types, yet they stay healthy.  Antibiotics are used when our bodies cannot
fight bacteria alone, therefore, antibiotic resistant bacteria are a real
problem.  However, people who cannot sufficiently fight bacteria cannot
fight the bacteria for a reason; antibiotics are not a cure, they are a
help.  The article also reported that: ‘Mortality from septicemia, a rapid
form of bacterial blood poisoning, increased 83 percent, and deaths from
respiratory tract infections rose 20 percent.  The increase in respiratory
deaths stems mostly from an aging population, but Pinner couldn’t explain
the septicemia increase.’  A younger population is dying from septicemia.”

The article of Jan 24 stated that ‘Anyone can get TB, but some people are at
higher risk such as: people with HIV, foreign-born people from countries
where a lot of people have TB, nursing home residents, prisoners and
alcoholics and intravenous drug users.’  According to my work, people of low
DHEA and high testosterone/low DHEA are more prone to infections.  People
with HIV are proven to be low in DHEA and men are more infected by the HIV
than other groups.  Nursing home residents are proven to be low in DHEA, and
the ones that require the most care have even lower DHEA (J. Am. Geriatric
Society 1990; 38: 421).  My work suggests people of high testosterone are
more impulsive; they commit more crimes.  This is why more men are in prison
than women and why more black men are in prison than white men (black men
produce significantly more testosterone, J. Nat. Cancer Institute 1986; 76:
421).  This also explains the ‘unexpected finding that under the same social
conditions, blacks are apparently infected more by Mycobacterium
tuberculosis than whites,’ (The New England Journal of Medicine 1990; 433:
422).  Aging people and the very young are also more vulnerable to
infections.  These are all groups of low DHEA, or low DHEA in addition to
high testosterone.”

The first quotation below is the quotation to which I referred above.  It is
also my hypothesis that the hormone, melatonin, interacts with DHEA in a
“melatonin-DHEA cycle.”  I think these two hormones interact in the
production of the other.  The second quotation below reports the very
similar finding that: “This is the first study to show that melatonin, which
is reported to be free of adverse side effects, can be considered a safe and
effective therapeutic agent for restoring the depressed immunological
function after soft-tissue trauma and hemorrhagic shock.”

Arch Surg 1998 Dec;133(12):1281-8
“Dehydroepiandrosterone: an inexpensive steroid hormone that decreases the
mortality due to sepsis following trauma-induced hemorrahage”
Angele MK, Catania RA, Ayala A, Cioffi WG, Bland KI, Chaudry IH
Center for Surgical Research, Department of Surgery, Brown University School
of Medicine, Rhode Island Hospital, Providence 02903, USA.

“BACKGROUND: Recent studies suggest that male sex steroids play a role in
producing immunodepression following trauma-hemorrhage. This notion is
supported by studies showing that castration of male mice before
trauma-hemorrhage or the administration of the androgen receptor blocker
flutamide following trauma-hemorrhage in noncastrated animals prevents
immunodepression and improves the survival rate of animals subjected to
subsequent sepsis. However, it remains unknown whether the most abundant
steroid hormone, dehydroepiandrosterone (DHEA), protects or depresses immune
functions following trauma-hemorrhage. In this regard, DHEA has been
reported to have estrogenic and androgenic properties, depending on the
hormonal milieu. OBJECTIVE: To determine whether administration of DHEA
after trauma-hemorrhage has any salutary or deleterious effects on immune
responses, and whether it improves the survival of animals subjected to
subsequent sepsis. DESIGN: Male C3H/HeN mice underwent laparotomy (ie,
trauma-induced) and hemorrhagic shock (blood pressure, 35+/-5 mm Hg for 90
minutes) followed by fluid resuscitation, or sham operation. The animals
then received 100 mg of DHEA (4 mg/kg) or propylene glycol (hereafter
referred to as vehicle). At 24 hours after trauma-hemorrhage and
resuscitation, the animals were killed and blood, spleens, and peritoneal
macrophages were harvested. Splenocyte proliferation and interleukin (IL) 2
release and splenic and peritoneal macrophage IL-1 and IL-6 release were
determined. In a separate set of experiments, sepsis was induced by cecal
ligation and puncture at 48 hours after trauma-hemorrhage and resuscitation.
For those studies, the animals received vehicle, a single 100-microg dose of
DHEA, or 100 microg/d DHEA for 3 days following hemorrhage and
resuscitation. Survival was monitored for 10 days after the induction of
sepsis. RESULTS: Administration of DHEA restored the depressed splenocyte
and macrophage functions at 24 hours after trauma-hemorrhage. Moreover,
daily administration of DHEA for 3 days significantly increased the survival
of animals subjected to subsequent sepsis (P=.01). CONCLUSION: The finding
that DHEA markedly improves the depressed immune functions and survival of
animals subjected to subsequent sepsis suggests that short-term treatment
with DHEA after trauma-hemorrhage is a safe and novel approach for
preventing immunodepression and for decreasing the mortality rate due to
subsequent sepsis.”

J Surg Res 1996 Jun;63(1):256-62
“Melatonin administration attenuates depressed immune functions
trauma-hemorrhage”
Wichmann MW, Zellweger R, DeMaso, Ayala A, Chaudry IH
Shock and Trauma Research Laboratories, Department of Surgery, Michigan
State University, East Lansing 48824-1315.

“The pineal hormone melatonin has been used in clinical trials in patients
suffering from AIDS and also as an adjuvant for cancer therapy. Although
melatonin has been reported to have beneficial effects in some animal models
of immune dysfunction, it remains unknown whether this hormone has any
salutary effects on immunity following soft-tissue trauma and/or major blood
loss. To study this, soft-tissue trauma (2.5-cm midline laparotomy) and
hemorrhagic shock (arterial BP 35 +/- 5 mm Hg) were induced in C3H/HeN mice.
The mice were resuscitated after 90 min of hypotension with the shed blood
and lactated Ringer's solution. Treatment with saline, vehicle, or melatonin
(10 mg/kg BW) subcutaneously was administered in the evening of the day of
surgery and again on the following evening. All animals were sacrificed at
48 hr following trauma-hemorrhage and resuscitation to obtain plasma,
splenocytes, as well as splenic and peritoneal macrophages (Mphi). The
results indicate that melatonin administration after trauma-hemorrhage
significantly improved the depressed immune functions, as evidenced by the
restoration of Mphi IL-1 and IL-6 release, as well as significantly improved
splenocyte IL-2 and IL-3 release and splenocyte proliferative capacity. No
differences in circulating corticosterone levels between vehicle- and
melatonin-treated animals were observed. This is the first study to show
that melatonin, which is reported to be free of adverse side effects, can be
considered a safe and effective therapeutic agent for restoring the
depressed immunological function after soft-tissue trauma and hemorrhagic
shock.”






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