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.)


Anthropogeny.com Copyright © 1985-2024 James Michael Howard, Fayetteville, Arkansas, U.S.A.  All rights reserved. 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.

The Impact of Dehydroepiandrosterone (DHEA) and Testosterone on Humans


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.)
 



Covid-19 Infection and Subsequent Pathology are Caused by


Low Dehydroepiandrosterone (DHEA)



(New support: Low DHEA in Covid-19)



(© Copyright 2020-2024, James Michael Howard, Fayetteville, Arkansas, U.S.A.)



New research, 2022, regarding DHEA has been published that supports my hypothesis that Covid-19 is caused by low DHEA: “COVID-19 patients with altered steroid hormone levels are more likely to have higher disease severity,” ( Endocrine volume 78 2022 Jul 30. doi: 10.1007/s12020-022-03140-6.) “DHEA was an independent indicator of the disease severity with COVID-19.”

It is my hypothesis that Covid-19 infection and subsequent pathology are caused by low levels of dehydroepiandrosterone (DHEA) which are affected by aging, testosterone and cortisol levels, and antagonism of DHEA by cortisol as in stress, all of which reduce effects of DHEA (© Copyright 2020, James Michael Howard, Fayetteville, Arkansas, U.S.A.). It is already known that DHEA provides protection from pathogenic viruses. “In this study it was shown that DHEA protects mice against WNV, SVNI and SFV lethal infection.” (Arch Virol. 1991;120(3-4):263-71. doi: 10.1007/BF01310481.) High testosterone levels affect DHEA levels by decreasing available DHEA by reducing conversion of DHEA sulfate to the active form, DHEA, and low testosterone levels reduce intracellular DHEA; both reduce DHEA. This is why high levels of testosterone in males and high levels of testosterone of blacks compared to whites increase Covid-19 virulence, therefore, drugs such as dexamethasone, which is known to reduce testosterone reduce Covid-19 This is why reduced DHEA and testosterone of aging increases Covid-19 virulence.

Regarding the “cytokine storm” in Covid-19 infection, a case may be made that these cytokines are produced by cells / tissues to stimulate DHEA production. Therefore, the reduction in DHEA caused by Covid-19 would cause numerous tissues to produce cytokines to stimulate DHEA. Individuals who do not recover significantly by eventually producing DHEA experience “long covid.”

This is derived from my explanation of human evolution involving DHEA (mammalian evolution) and human evolution involving DHEA and testosterone. I suggest testosterone directly affects levels of DHEA and testosterone is increasing throughout human history and is ongoing. At this time I think testosterone has increased in human populations sufficiently to adversely affect DHEA levels. I suggest this is why human populations are experiencing increases in obesity, type 2 diabetes, cancer, infections, at this time, including Covid-19. (Note: some consider obesity as the cause of the others; obesity is simply the earliest sign.)

Since I think these androgens and their ratio control all aspects of the human life span, I think they are involved in all aspects of normal ontogeny as well as pathology. I suggest this is why Covid-19 has been connected with many pathologies as well as disturbances in cytokines, including “hypertension, diabetes, obesity, COPD, and CVD.”

As I stated above, I think testosterone is increasing with time within populations; an over abundance of testosterone can reduce the effects of DHEA and this is why pandemics are occurring, such as the HIV and others at this time. This is why Covid-19 is occurring at this time and is directly connected to other pathology. They are both caused by low DHEA.

“Hormones in Mammalian Evolution,” Rivista di Biologia / Biology Forum 2001; 94: 177-184. If your library does not subscribe to “Rivista … ,” you may find this at: http://anthropogeny.com/Hormones%20in%20Mammalian%20Evolution.htm .

Androgens in Human Evolution, Rivista di Biologia / Biology Forum 2001; 94: 345-362. If your library does not subscribe to Rivista , you may find this at: http://anthropogeny.com/Androgens%20in%20Human%20Evolution.htm where you may also see a chart of testosterone in humans and great apes which directly supports my hypothesis and was reported in the literature 2 years later.

New connections of low DHEA and Covid-19, January, 2023: Low DHEA has been found in “burning mouth (BM),” (Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2009 Oct;108(4):537-43. doi: 10.1016/j.tripleo.2009.06.022. PMID: 19778740.). “Glossodynia [burning mouth] is significantly more common in COVID-19 patients and should be considered in the differential diagnoses among the oral complications of this infection.” (Am J Dent 2022;35:9-1. 2022 Feb;35(11) :9-11





I invite you to read my explanation of Down’s Syndrome which includes a direct explanation of the connection of maternal age in the etiology.





Down's Syndrome, Trisomy 21, Dehydroepiandrosterone (DHEA), and DNA Methylation: a Possible Explanation


© Copyright 2020 James Michael Howard, Fayetteville, Arkansas, U.S.A.

The cause of Down's syndrome (DS) may be low levels of maternal dehydroepiandrosterone (DHEA) in utero.  This includes DNA associated characteristics as well as the chromosome 21 aneuploidy.  ("DHEA supplementation to a significant degree reduced number (P = 0.029) and percentages (P < 0.001) of aneuploid embryos, adjusted for relevant covariates. Short term supplementation (4-12 weeks) resulted in greatest reduction in aneuploidy (21.6%, 95% CI -2.871-46.031)." Reprod Biol Endocrinol. 2010; 8: 140.
Published online 2010 Nov 10. doi: 10.1186/1477-7827-8-140  )  DHEA naturally peaks around ages of 20-25 years, declining, thereafter, to very low levels in old age.  DS is characteristically found in offspring of women 35-years-old or later.  The “DNA associated characteristics” are the basis of my explanation of DS.  (This is derived from my explanations of mammalian and human evolution; citations for these are at the end of this treatise.)

I think DHEA is directly involved in all DNA, gene, activity.   A ratio of DHEA and DNA is disturbed by increased DNA, extra chromosome 21, in Down’s syndrome, that is, the ratio of DHEA to DNA is reduced.  This may be demonstrated by DNA methylation patterns.  I first suggested DHEA is involved in DNA methylation in 2015.  "I suggest DNA methylation is an evolutionary consequence of reduced levels of dehydroepiandrosterone (DHEA) and is involved in cancer initiation." ("DNA Methylation, DHEA, and Cancer," http://anthropogeny.com/DNAmethDHEAcancer.html  )  Again, DHEA naturally begins to decline in women around ages 20-25. reaching very low levels in old age; I suggest it is the low DHEA of women around age 35 that is the cause of Down syndrome.  Low DHEA has been reported in Down's syndrome J Neuroendocrinol. 2011 May;23(5):450-5. doi: 10.1111/j.1365-2826.2011.02118.x ).

A study of DNA methylation in DS reported that "Overall, our results indicate that the chorionic villi cells of DS [Down syndrome] fetuses are hypermethylated in all autosomes and suggested that altered DNA methylation may be a recurrent and functionally relevant downstream response to DS in human cells."  ( Clin Epigenet 11, 180 (2019). https://doi.org/10.1186/s13148-019-0756-4 ).  This means that all of these chromosomes may be affected by the low DHEA to DNA ratio in DS.

I suggest the low ratio of DHEA to DNA is the cause of Down’s syndrome aneuploidy and the resultant characteristics of Down's syndrome.  Measurements of, and adjustment thereof, DHEA in pregnant women, or those intending to become pregnant, should be performed on all women.  (For sake of support, low DHEA in young women has been determined to reduce pregnancies.)


“Hormones in Mammalian Evolution,” Rivista di Biologia / Biology Forum 2001; 94: 177-184.  If your library does not subscribe to “Rivista … ,” you may find this at: http://anthropogeny.com/Hormones%20in%20Mammalian%20Evolution.htm .

“Androgens in Human Evolution,” Rivista di Biologia / Biology Forum 2001; 94: 345-362.  If your library does not subscribe to “Rivista … ,” you may find this at: http://anthropogeny.com/Androgens%20in%20Human%20Evolution.htm where you may also see a chart of testosterone in humans and great apes which directly supports my hypothesis and was reported in the literature 2 years later.




                                   Covid-19 is Cause of Current Increased Virulence

of RSV and Influenza



(© Copyright 2022 James Michael Howard, Fayetteville, Arkansas, USA)

I suggest the basis of increased virulence of Respiratory Syncytial Virus and influenza at this time is reduction of dehydroepiandrosterone (DHEA) caused by Covid-19. It is my hypothesis that Covid-19 infection and subsequent pathology are caused by low DHEA. Support of low DHEA associated with Covid-19 virulence has recently been reported. It has been determined that DHEA stimulates / increases antibody formation in aged mice: “When DHEA was provided either topically or was incorporated directly into vaccine, vigorous primary and secondary antibody responses were detected in the aged mice given a single administration of DHEA, regardless of the mode of administration.” (The Journal of Infectious Diseases No. 4 (Apr., 1993), pp. 830-840 ).

I submit the Covid-19 pandemic has reduced DHEA throughout the world, which has reduced the antibody response to RSV and influenza. I suggest this is the cause of the ongoing increase in RSV and influenza. This may also explain the common increase in Covid-19, influenza, and RSV in the United States at this time. We may have discarded our prophylaxis of Covid-19 infection too early.

Further support and regarding the current increase in Respiratory Syncytial Virus: It has been reported that “High PRL [prolactin] serum level or hyperprolactinemia is associated with different viral infections.” (Mol Cell Biochem 477, 1381–1392 (2022). https://doi.org/10.1007/s11010-022-04381-9 )

Prolactin is a direct and specific stimulant of DHEA; high PRL indicates an immune response to increase DHEA. “there seems to be a correlation between prolactin signalling and severity of infection [RSV]” (“Respiratory syncytial virus (RSV): a scourge from infancy to old age,” BMJ “Thorax” https://doi.org/10.1136/thoraxjnl-2018-212212 )





… and the increase in AUTISM RATES reported around January 25, 2023. … another case of effects of low dehydroepiandrosterone (DHEA) caused by Covid-19.  (© Copyright 2023, James Michael Howard, Fayetteville, Arkansas USA)

It is my hypothesis of 2003 that high maternal testosterone causes Autism by reducing available DHEA for growth and development of the brain. “The Increase in Autism in California (which [was] is also occurring in other areas),” https://anthropogeny.com/increase%20in%20autism.htm . At the time a large increase in autism frequency was being reported in California. It was also considered to be by enhanced diagnoses. I explained that a mother of high testosterone uses available DHEA at the expense the child and that the 2003 autism increase in California was caused by increased maternal testosterone within the population.
I am suggesting here that Covid-19 reduced these mothers’ DHEA which is causing increasing autism at this time.
My identification of high maternal testosterone has recently been supported.
“SARS-CoV-2 infection indicated an increased risk of preterm delivery (p<0·05) and stillbirth (p<0·05), accounted for primarily by first and second trimester SARS-CoV-2 infections.” (“The effect of maternal SARS-CoV-2 infection timing on birth outcomes: a retrospective multicentre cohort study,” (he Lancet Digital Health, ISSN: 2589-7500, Vol: 4, Issue: 2, Page: e95-e104
Publication Year2022 )
“Findings provide support for direct involvement of maternal hyperandrogenemia in ASD [autism spectrum disorder] etiology. Alternatively, findings might reflect shared genetic and/or environmental factors independently affecting maternal androgen homeostasis and fetal neurodevelopment.” (“Associations of Maternal Androgen-Related Conditions With Risk of Autism Spectrum Disorder in Progeny and Mediation by Cardiovascular, Metabolic, and Fertility Factor,” American Journal of Epidemiology, Volume 190, Issue 4, April 2021, Pages 600–610



Human Evolution is Caused by Increased Testosterone / Dehydroepiandrosterone (DHEA) resulting in Increased Myelin which is the Cause of Increased Brain Structure and Function ... Bigger, Faster Brains


© 2024 Copyright James Michael Howard, Fayetteville, Arkansas, USA


It is my hypothesis mammalian evolution occurred because of selection for DHEA and human evolution occurred because of selection for testosterone because it increases intracellular DHEA primarily in the brain. I suggest this occurred in Homo erectus females. It is visible in the fossil record; sexual dimorphism diminished in erectus when females increased in size without change in male size and caused "gracilization," in hominids wherein brain size increased at the expense of body size, a hallmark of hominid evolution. The effect occurs in utero, and is mainly effective during "minipuberty," which occurs at birth. Minipuberty is characterized by a large production of testosterone at birth. Most literature reports concerning minipuberty suggest this period is designed for testiscular development. Since I think the testosterone / DHEA synergy evolved for general cellular growth and development, I agree with this: "During mini-puberty, males' external genitalia is more related to somatic growth than to reproductive hormones, but this relationship is not observed in girls." (Eur J Pediatr (2023). https://doi.org/10.1007/s00431-023-05393-3 ).

The large production of testosterone at minipuberty causes the large, available DHEA to enter cells to stimulate growth and development ... of myelin. Female testosterone increased in female Homines erecti and they were selected by males.This causes DHEA to literally be used one; hence the large decline of DHEA of Period A.

I think the foregoing increases the effects of minipuberty on early brain growth and development and myelin. Increased myelin is the basis of our larger, faster brains.

Myelin is directly affected by testosterone and DHEA. Every aspect whereby we, as enhanced testosterone producers and males and females, shows the positive effects of testosterone / DHEA on myelin.

"Comparative studies have noted that the white matter tends to take up more and more space in larger-sized brains compared with smaller brains. The proportion of white matter to total brain volume ranges from an estimated 11% in mice to 27% in macaques to 40–41% in chimpanzees and humans" (Logo of cercor

Cereb Cortex. 2022 Jul 1; 32(13): 2831–2842. Published online 2021 Nov 24. doi: 10.1093/cercor/bhab384)

For sake of brevity, I suggest human evolution occurred because of increases in testosterone and DHEA which produce increases in myelin and myelin effects. (The literature is replete with effects of myelin and differences in myelin that support my foregoing hypothesis. Look it up.)

("Hormones in Mammalian Evolution," Rivista di Biologia / Biology Forum 2001; 94: 177-184. If your library does not subscribe to "Rivista ... ," you may find this at: https://anthropogeny.com/Androgens%20in%20Human... )

(Androgens in Human Evolution, Rivista di Biologia / Biology Forum 2001; 94: 345-362. If your library does not subscribe to Rivista , you may find this at: https://anthropogeny.com/Androgens%20in%20Human... where you may also see a chart of testosterone in humans and great apes which directly supports my hypothesis and was reported in the literature

This chart represents the availability of DHEA during the human life-span. (It is derived from two separate charts which I have combined from “Adrenal Androgens,” A.R. Genazzani, Raven Press, 1980.) (I was able to post the chart just above this.) Period A is the first postnatal year (MINIPUBERTY), Period B is a period of very low DHEA, Period C is the rise of DHEA of childhood prior (adrenarche) to the onset of puberty, Period D is the reproductive period, Period E and F are early and late aging. This chart represents the availability of DHEA during the human life-span. (It is derived from two separate charts in Adrenal Androgens, A.R. Genazzani, Raven Press, 1980.)

I suggest what I call “A” is minipuberty. Testosterone increases postpartum in minipuberty. As I stated above, I think testosterone increases DHEA primarily in the brain. “A” demonstrates the large decline of DHEA because of the testosterone. DHEA, I suggest, is literally “used up” in stimulating myelin. (I will add these connections of myelin characteristics of the brain soon; I submit it is this powerful stimulation of testosterone and DHEA that “causes” Homo sapiens.

"A peak of myelination is observed during the first post-natal year." (Neuroimage. 2019 Jan 15; 185: 349–360.

Published online 2018 Oct 10. doi: 10.1016/j.neuroimage.2018.10.031 ) The chart of life span of DHEA shows a very large amount of DHEA at birth which falls dramatically during the first year which is, I suggest, used during this dramatic increase in myelin.

"Throughout early neurodevelopment, myelination helps provide the foundation for brain connectivity and supports the emergence of cognitive and behavioral functioning." (Neuroimage. 2018 Sep; 178: 649–659. Published online 2017 Dec 20. doi: 10.1016/j.neuroimage.2017.12.056 )