Testosterone and DHEA Levels are Involved in the Epidemiology and
Current Increase in Asthma

Copyright 2005, James Michael Howard, Fayetteville, Arkansas, U.S.A.

It is my hypothesis that the "secular trend," the increase in size and
earlier onset of puberty in children, is caused by an increase in the
percentage of individuals of higher testosterone within a population
over time.  Individuals of higher testosterone will be more
aggressive, impulsive, and sexual than individuals of lower
testosterone; they will reproduce faster.  Some say the trend is
caused by increased calories.  Increased calories does not cause the
trend, increased calories simply increase reproduction.  The increase
in testosterone may cause the secular trend and the increase in
asthma, among other disorders.  This effect would be stronger in
developed countries because of increased calories.

The key to understanding my hypothesis is that testosterone reduces
the conversion of dehydroepiandrosterone sulfate (DHEAS), the
background source, to DHEA.  Low DHEA, or less available DHEA, may be
the source of asthma.  Dr. Platts-Mills points out "the persistent
Association between specific IgE, total IgE, and asthma."  Asthma is
connected to increased IGE.  DHEA lowers IGE in mice (Immunol Lett.
2001 Dec 3;79(3):177-9 and Clin Exp Allergy. 1999 Mar;29(3):414-22).
DHEA is very low in young children, begins to increase around age five
reaching a peak around age twenty to twenty-five, then begins to
decline to very low levels in old age.  This pattern of DHEA
production would fit explain some of the epidemiology of asthma,
especially if one includes the effects of testosterone in both sexes
along with a similar effect of estradiol on DHEA in females.  The
decline of DHEA in the elderly may explain why IGE increases in
elderly people with asthma (Allergy Asthma Proc. 2004
Sep-Oct;25(5):321-5).  Environmental smoke and obesity has been
connected with childhood asthma.  Smoking and obesity have been
connected with reductions in DHEA.  DHEA is known to be low in HIV /
AIDS and IGE levels increase with progression of AIDS (Rev Alerg Mex.
2004 Mar-Apr;51(2):54-60).

Blacks produce more testosterone than whites.  Blacks consistently
exhibit more asthma than whites (Chest. 2003 Sep;124(3):803-12).  I
suggest this difference in asthmatic rates may be a result of greater
testosterone in blacks reducing the availability of DHEA.  It is also
my hypothesis that increased maternal tesoterone is the cause of many
adverse pregnancy outcomes, besides asthma.  In undeveloped countries
the outcomes of these pregnancies probably result in stillbirth or
neonatal death.  Once "cleanliness" is instituted, this trend may be
decreased.  This could result in an increase in the percentage of
children exposed to high levels of maternal testosterone living and
developing asthma.

I suggest testosterone and the effects of testosterone on
dehydroepiandrosterone may explain the epidemiology of asthma and the
current increase in asthma worldwide.