Testosterone and DHEA Levels are Involved in the Epidemiology and Current Increase in Asthma
Copyright 2005, James Michael Howard,
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.