Our COVID-19 Pandemic May be Caused by Early Decline of the Crucial DHEA / Testosterone Receptor.
testosterone levels species
The Biological Secular Trend in America ...and Elsewhere. This IS what will really affect us!
A syndrome is occurring in America and other countries, the cause of which is often attributed to one part or another of the syndrome, itself, and more often attributed to the environment or life style.  This is the “secular trend.”  The secular trend is / has been attributed to increased calories or genetics.  I suggest a single cause may be involved that it is biological, epigenetic, and evidence of ongoing human evolution.  The cause is increased exposure to high maternal testosterone within the population with time.  This increase in testosterone produces a change in the other, major androgen, dehydroepiandrosterone (DHEA), because testosterone increases differential tissue competition for DHEA and interferes with steroid sulfatase.  If the precursor of DHEA, DHEAS[sulfate], is not converted to DHEA, DHEA availability is reduced.  It is the reduction in DHEA that is the basis of these problems.  High DHEAS is often found with high testosterone.  A consequence of this is reduced availability of DHEA (just above) and an earlier decline in the production of DHEA during the life span.  This produces increased morbidity during life, as well as earlier mortality, and intellectual and behavioral reductions in the population, all of which are increasing simultaneously.  That is, all gene expression is being affected simultaneously.

I think mammals evolved because of evolutionary selection for DHEA.  Within mammalia, testosterone was subsequently selected because of its effects on distribution and use of the “mammalian producing effects of DHEA” in differing tissues.  The most radical change was the increased use of DHEA by the brain.  This increased neurological absorption of DHEA by the brain for growth and development, at the expense of the postcranial body.  Hence, human evolution is marked by reduced “robustness” of the bodies of hominids as the brain increased in size.  (“Hormones in Mammalian Evolution,” Rivista di Biologia / Biology Forum 2001; 94: 177-184.) This increase in testosterone produced the “Primates,” which finalized in human evolution.  (“Mitochondrial Eve,' 'Y Chromosome Adam,' Testosterone, and Human Evolution,” Rivista di Biologia / Biology Forum 2002; 95: 319-326.)  This is why we obviously are mammals but the great apes are more like us.

It is my hypothesis that human evolution is driven by increases in testosterone ("Androgens in Human Evolution," Rivista di Biologia / Biology Forum 2001; 94: 345-362; http://anthropogeny.com/Androgens%20in%20Human%20Evolution.htm ).  This was directly supported by research in 2003 regarding testosterone levels in humans and the great apes (following chart).  This increase in testosterone, during pregnancy, caused / causes effects on utilization. 

It is my hypothesis that the "secular trend," the increase in size and earlier puberty occurring in children, is caused by an increase in the percentage of individuals of higher testosterone. More specifically, I suggest this is due to an increase in the percentage of mothers of higher testosterone with time within the population. This exposes more fetuses to increased maternal testosterone with time within the population. This causes permanent effects in the fetus which persist throughout the life span.  I suggest this is the cause of the parallel increases in morbidity occurring within the population, such as increased infection rates, autism, obesity, hypertension, chronic obstructive pulmonary disease (COPD), cancer, breast cancer, diabetes, the metabolic syndrome, etc., including prematurity, small for gestational age, etc., including less obvious gross effects which later contribute to "failing schools" and other adverse behavioral outcomes in children.  This includes the (August,2011) finding of Dr. Kyung Hee Kim of The College of William and Mary that "creativity" is also declining in children.  Earlier puberty is caused by increased activity of the “limbic” brain with less development of the prefrontal lobes.  Reduced development of the prefrontal lobes, much more developed in humans than the great apes, reduces intelligence and reduces impulse control.

I suggest that periodically testosterone increases excessively and the exposure to excessive maternal testosterone causes negative and evolutionarily consequential changes to the human population.  We are experiencing this effect at this time.

Without the foregoing explanation and looking only at statistics, one may arrive at unwarranted conclusions.  For example, this could also explain the increase in negative pregnancy outcomes, re: the increase in the increasing "newborn death rate" in the United States, vis-à-vis, perhaps the one of the best, maybe the best, medical training systems in the world.  (“High incidence of negative pregnancy outcomes” is a not a consequence of substandard medicine in the United States, as it is often portrayed, but an indication that the secular trend is highest in the U.S.  “Explanation of Preterm and Reduced Growth and Development,” at: http://anthropogeny.com/Preterm%20and%20Reduced%20Growth%20and%20Development.html

I suggest this increase in testosterone in the population peaks earlier with time.  This earlier peak may produce an earlier decrease in the population with aging.  A number of studies reported in the medical literature have identified low testosterone as a cause of currently increasing disorders.  Therefore, the secular trend may be causing increased morbidity and mortality as a result of excessive testosterone and low testosterone within the population.  Earlier reductions in testosterone and DHEA could be occurring simultaneously, therefore, reducing the total positive effects of these two major androgens.  This could be the explanation of the severe increase in morbidity that is occurring.  Evolution is increasing earlier reproductive capacity at the expense of post-reproductive years.  The curve of the peak of our androgens is being "skewed to the left."

As I have said elsewhere, I think women of higher testosterone drive the secular trend / human evolution.  I suggest these women produce the highest percentage of premature infants. It has been reported that "preterm boys" exhibit increased testosterone and the effects of increased testosterone compared to "full term boys" (J Clin Endocrinol Metab 2010, "Increased Activity of the Hypothalamic-Pituitary-Testicular Axis in Infancy Results in Increased Androgen Action in Premature Boys.," Kuiri-Hanninen, et al., J Clin Endocrinol Metab. 2011 Jan;96(1):98-105). What this means is that the population is increasing in women of higher testosterone and this group of women may also be increasing the percentage of men of higher testosterone simultaneously. This could explain why this "secular trend" can increase so rapidly. This mechanism could expand the percentage of these individuals within a population rapidly and drive human evolution.

During the past couple of years, some of the components of the trend have slowed or become stable.  These are reported in the media as examples of hoped-for changes in behavior of the individuals involved.  While, admittedly, I hope these may be real, I doubt it. 

Women of higher testosterone exhibit reduced fertility. In the absence of clinical signs of hyperandrogenism. In other words, increased testosterone may reduce fertility in women and girls without outward signs of excessive testosterone. The mean level of free T [testosterone] was significantly higher (P less than 0.05) in anovulatory women when compared with ovulatory ones. .The results show that in infertile women determination of androgen levels, and especially free T [testosterone], is indicated in the absence of clinical signs of hyperandrogenism. (Human Reproduction 1988; 3: 437-439).  In men, high testosterone can reduce fertility.

This means that sociological / environmental attempts to curb various aspects of the secular trend may be only illusory.  Ironically, the mechanism of the secular trend may produce a plateau of amount of effects.  I suggest this may be why older countries may exhibit these plateaus or even some retroactive reductions in the secular trend.

For a more detailed explanation of the interaction of testosterone and dehydroepiandrosterone (DHEA) and the importance of these androgens to the secular trend: “ DHEA, Estradiol, Testosterone, and the Relevance of Their Ratio …The Androgen Receptor …and the Secular Trend,” at:
 My explanation of:


...what it is and when and where it exists in the literature and the internet.

DHEA During Human Lifespan

Period "B" is adrenarche.
I suggest the occurrence of many diseases is dependent upon the decline of DHEA which begins around 20-25 years of age and reaches very low levels in old age.  Also, it follows from my work, that many problems that are increasing with time in the United States and in the world are resulting from the "secular trend," which I suggest is due to the increase in percentages of individuals of higher testosterone and the negative effect that testosterone exerts on the availability of DHEA.  Disturbances in "dehydroepiandrosterone homeostasis" may be a significant source of morbidity and mortality.
(Copyright 2003, James Michael Howard, Fayetteville, Arkansas, U.S.A.)
it is like a wall...
it is like a snake
Copyright © 1985-2020 James Michael Howard, Fayetteville, Arkansas, U.S.A. 
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  All pages are under construction and updated periodically due to new research.  Nothing is sold at this site nor is any product or service endorsed anywhere.

Modern applications extends my work to modern humans.  “Modern humans” is a very broad area since it includes Homo sapiens from our origin in Africa through today.  Human evolution is ongoing and identifiable within current populations.
New Ideas and Research contains current research of relevance to this site.  This includes applications of my work to new research.  These explanations will both extend and revise my past work.  These interpretations will be moved to the other sections below as necessary.
Physiology and Pathology is the broadest category.  This area contains many aspects of growth, development, and aging, as well as significant deviations from normal.  This concerns our individual lives or ontogeny.
Evolution  includes an examination of evolution primarily concerned with human phylogeny.  This extends from evolution of eukaryotic organisms to humans.

  1. This site is intended to disseminate information generated from ongoing work I began in 1984.  Two works were produced in 1985: Evolution of Sociopathy in Western Civilization. A Philosophical Treatise followed by A Theory of the Control of the Ontogeny and Phylogeny of Homo sapiens by the Interaction of Dehydroepiandrosterone and the Amygdala, both copyrighted.  The original focus was narrow.  The scope has rapidly broadened simultaneously with increasing awareness of the explanatory usefulness of the primary ideas.  It is my hypothesis that selection for the androgens, dehydroepiandrosterone and testosterone, is directly linked to human evolution.  Evolution consists of ontogeny and phylogeny.
The information is divided into categories variously dealing with human ontogeny and phylogeny.  Since human ontogeny, the life of the individual, and phylogeny, the life of the species, are interdependent, my divisions are also not exclusive.  These categories are intended only as different entrances to a single explanation of human biology.  There is extensive overlap.  Periodically, new research will be included and discussed below.  (Click on the appropriate category below to access the page.)

Anthropogeny is the study of human ontogeny and phylogeny.

The Impact of Dehydroepiandrosterone (DHEA) and Testosterone on Humans

(Since the beginning of this work, 1984, I have had some difficulty combining some data regarding DHEA with data regarding testosterone.  I now think evolution selected these two androgens, through mammalian and human evolution, to work together in a manner which produces different effects according to their relative ratios.  For a more detailed explanation of the interaction of testosterone and dehydroepiandrosterone (DHEA) and the importance of these androgens to the secular trend: “ DHEA, Estradiol, Testosterone, and the Relevance of Their Ratio …The Androgen Receptor …and the Secular Trend,” at: http://anthropogeny.com/Androgen%20Receptor%20and%20Secular%20Trend.htm .)  Until I am able to apply this to my earlier work, the foregoing reference may apply to some of my hypotheses.)

(Note: At this time, most of my most recent posts are located just below; others in "Modern Applications," the link is found below.)

 "An Explanation of Increasing Childhood and Adult Obesity Caused by a Single Mechanism"

New Research, May, 2015, may Prove my Explanation of Autism

Dehydroepiandrosterone, Sleep, and DNA Methylation

DNA Methylation, Dehydroepiandrosterone, and Cancer

Complement Component C4 and Schizophrenia

Talcum Powder, Testosterone, and Ovarian Cancer

Testosterone Controls Human and Great Ape Lifespans {New Support)

Consequences of the Ongoing Secular Trend

DHEA may be the Natural Ligand of Cannabinoid Receptors as well as Androgen and Estrogen Receptors

A Possible Explanation of Multidrug Resistant Cancer: Low Dehydroepiandrosterone (DHEA) and High Prolactin

Testosterone and Nausea

Use Of DHEA By Cancer Explains The "Warburg Effect" ...Increased Cancer Metabolism (New Support of Cancer Explanation)

DNA Mutations, Cancer, and Cell Divisions

A Synopsis of the Basis of Type 2 Diabetes Based on Testosterone, Dehydroepiandrosterone (DHEA), and Glucose Transporter Genes

New support of my "Telomeres, Telomerase, Dehydroepiandrosterone, and Cancer and Aging," of 2004 at: http://anthropogeny.com/Telomeres.htm . " "Impact of Dehydroepiandrosterone Sulfate on Newborn Leukocyte Telomere Length," Scientific Reports 2017, Liu, et al., at: https://www.ncbi.nlm.nih.gov/pubmed/28186106 directly adds new support to my 2004 report.

More new at "James Michael Howard" on Facebook (red jacket, white hat)

Explanation of Negative Pathology in Older Childhood / Adulthood caused by Radio- and Chemotherapy of Childhood Cancers: Reduced testosterone and Dehydroepiandrosterone (DHEA) and Why This Effect is Decreasing

How NOX4 Affects Cancer Formation: New Support of My Explanation of the "Warburg Effect," the Increase of Metabolism in Cancer

Castleman's Disease, Interleukin 6, and Dehydroepiandrosterone Castleman's disease.htmlndrosterone (DHEA)

Our COVID-19 Pandemic May be Caused by Early Decline of the Crucial DHEA / Testosterone Receptor.