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

Low Dehydroepiandrosterone (DHEA), a known, natural antiviral agent, May be Directly Involved in COVID-19 Infection, Pathology, and Morbity.


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





http://anthropogeny.com/MAINCUR.jpg





DHEA during the human life span.



The epidemiology of COVID-19 follows DHEA levels in humans. In this chart of DHEA from birth to death, levels of DHEA are high at birth and for a short time thereafter (newborns) (Period A). DHEA then declines to low levels (Period B), then increases (Period C and D) until it begins to decline Periods D, E, and F) reaching very low levels in old age. COVID-19 pathology is highest during periods of low DHEA (Periods B, somewhere in Period D, depending upon one’s personal production, Period E, and Period F); early childhood, early decline of adulthood and old age. This is why infancy exerts protective effects while early childhood does not.

Cases of coronavirus disease 2019 (COVID-19) among children in China have been less severe than those in adults, according to a new study.

However, being in a young age group wasn’t entirely protective. Infants had higher rates of severe illness than older children. Experts also say more testing and research will be needed to understand childrens role in spreading the virus in their communities.”

( https://www.aappublications.org/news/2020/03/16/coronavirus031620 )


COVID-19, Interleukin-6, and DHEA:


It has been determined that interleukin-6 levels directly parallel COVID-6 ...”drastically elevated interleukin 6 (IL-6) level in critically ill COVID-19 patients,”(https://doi.org/10.1101/2020.02.29.20029520 ) and “Serum Dehydroepiandrosterone (DHEA) and DHEA Sulfate Are Negatively Correlated with Serum Interleukin-6 (IL-6), and DHEA Inhibits IL-6 Secretion from Mononuclear Cells in Man in Vitro: Possible Link between Endocrinosenescence and Immunosenescence” The Journal of Clinical Endocrinology & Metabolism, Volume 83, Issue 6, 1 June 1998, Pages 2012–2017, https://doi.org/10.1210/jcem.83.6.4876


I suggest a case may be made that DHEA, a known antiviral agent, levels are directly involved in protection from the COVID-19 in infants.


"A novel viral respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is responsible for an epidemic of the coronavirus disease 2019 (COVID-19) in cases in China and worldwide. Four full-term, singleton infants were born to pregnant women who tested positive for COVID-19 in the city of Wuhan, the capital of Hubei province, China, where the disease was first identified. Of the three infants, for who consent to be diagnostically tested was provided, none tested positive for the virus. None of the infants developed serious clinical symptoms such as fever, cough, diarrhea, or abnormal radiologic or hematologic evidence, and all four infants were alive at the time of hospital discharge." (Frontiers Pediatrics, 16 March 2020 | https://doi.org/10.3389/fped.2020.00104 )


It has been determined that "Preliminary evidence suggests children are just as likely as adults to become infected with SARS-CoV-2 but are less likely to be symptomatic or develop severe symptoms." "Preliminary evidence suggests children are just as likely as adults to become infected with SARS-CoV-2 but are less likely to be symptomatic or develop severe symptoms." (The Pediatric Infectious Disease Journal: March 12, 2020 - Volume Online First - Issue -

doi: 10.1097/INF.0000000000002660 ). (I have notified the authors of this possible explanation.)


"I suggest the basis of these findings is higher dehydroepiandrosterone (DHEA) in children compared to adults. DHEA is known to reduce virulence of many infections, including viral infections. DHEA is the active molecule which is made from the inactive, DHEA sulfate (DHEAS). Testosterone is known to reduce sulfatase which reduces DHEA availability from DHEAS. I suggest this is the reason that children exhibit less effects from coronavirus infections compared to adults, that is, individuals post pubertal. Furthermore, DHEA naturally begins to decline around ages of 20-25, reaching very low levels in old age. This would explain the increased virulence in adults, especially in old age.


It is my hypothesis that human evolution is driven by increases in testosterone. This would explain why infectious agents are entering the human population from other animals as our testosterone increases. (Human testosterone is much higher and DHEA much lower than in chimpanzees and other great apes. Currently, it is thought that "simian immunodeficiency virus or SIV" mutation gave rise to the HIV, which increased because of monkey meat consumption. As testosterone increases in humans, DHEAS increases. So, like the HIV, coronavirus enters our population as we increase testosterone and reduce DHEA. Human testosterone testosterone begins to increase in the fall and winter, and influenza activity often increases in October.


Again, I suggest the basis of these findings that children exhibit reduced COVID19 virulence is higher DHEA in children. This immediately suggests that treatment with DHEA should be available to aging adults as their DHEA naturally declines with age.


Smoking, Males, and COVID-19: It has been reported that male sex and smoking increased the probability of infection. This, again, can be explained by low DHEA levels. Smoking increases testosterone levels which have a negative effect on DHEA availability. Testosterone decreases sulfatase activity, that is, it reduces conversion of DHEA sulfate to the active form, DHEA. Throughout this treatise I have been suggesting that low DHEA is at the center of infection / symptomology of COVID-19. This may explain why males and smoking may be connected to COVID-19


(Note: It is known that DHEA protects against West Nile Virus (J Med Virol. 1992 Nov;38(3):159-66. In fact, “A significant protective effect of a native adrenal steroid, dehydroepiandrosterone (DHEA), was demonstrated in studies of two lethal viral infection models in mice: systemic coxsackievirus B4 and herpes simplex type 2 encephalitis. … While the molecular basis for DHEA's effect on the immune system is not known, studies by others suggest that it may counteract the stress related immunosuppressive effects of glucocorticoids stimulated by viral infection. … Because DHEA is a native steroid that has been used clinically with minimal side effects, the utility of DHEA in the therapeutic modulation of acute and chronic viral infections including the acquired immune deficiency syndrome deserves intensive study.” (Journal of Medical Virology Volume26, Issue3 November 1988 Pages 301-314 https://doi.org/10.1002/jmv.189026031)


(Note: It is my hypothesis that DHEA evolved to work with testosterone because it stimulates androgen receptors through which intracellular DHEA is stimulated. Therefore, the natural decline of testosterone of aging combines to increases the reduction of intracellular DHEA with aging. These two androgens work together. This is why treatment of older individuals with either DHEA or testosterone alone, often do not produce significantly positive results. This is partly derived from ("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.)"