It is my hypothesis that increased testosterone increases HIV infection rates and AIDS . This will explain why AIDS is so high in Africa. Blacks produce more testosterone than whites, and the infection rate of blacks far exceeds the rate in whites. (Blacks males produce significantly more testosterone than while males, (J Natl Cancer Inst 1986; 76: 45), and black females produce more testosterone than white females, (J Clin Endocrin Metab 1996; 81: 1108). In the following quotations regarding establishment of a virus, equine arteritis virus (EAV) in horses, it is demonstrated that testosterone is directly involved in infection and maintenance of the EAV. It has been determined that: "The findings confirm that persistent EAV infection is unlikely to occur in geldings and support the results of previous studies, which demonstrated that testosterone plays an essential role in the establishment and maintenance of the carrier state." (J Comp Pathol 1994; 111: 383, first quotation below). Also: "These findings confirm that the virus can replicate in the reproductive tract of a significant proportion of colts for a variable period of time after clinical recovery in the absence of circulating concentrations of testosterone equivalent to those found in sexually mature stallions." (J Comp Pathol 1993; 109: 29 , second quotation below). I suggest the same influence of testosterone is occurring in the infection rate of HIV, and resultant AIDS, in high testosterone people, that is, blacks.

McCollum WH, et al., "Resistance of Castrated Male Horses to Attempted Establishment of the Carrier State with Equine Arteritis Virus," (J Comp Pathol 1994; 111: 383).

"Twelve geldings all became infected when inoculated intranasally with the KY-84 strain of equine arteritis virus (EAV), a strain previously shown to be capable of establishing the carrier state in the stallion. With the exception of one animal that showed no effects other than pyrexia, all of the geldings developed clinical signs characteristic of equine viral arteritis (EAV). The geldings were febrile for varying periods within the range of 2-10 days after inoculation. Viraemia occurred from day 2 onwards, for periods varying from 9 to at least 19 days. Nasal shedding of virus began 2-4 days after inoculation and persisted for periods ranging from 7-14 days. All geldings "seroconverted" to EAV by day 11, with serum neutralization titres ranging from 8 to 64. The titres ranged from 8 to 32 after 4 weeks. Low concentrations of EAV were detected in the kidney and blood of one gelding killed 30 days after inoculation and in the blood of another killed after 57 days. Virus was not isolated from any tissue or fluid collected from the remaining 10 geldings, all of which were killed between days 30 and 148. The findings confirm that persistent EAV infection is unlikely to occur in geldings and support the results of previous studies, which demonstrated that testosterone plays an essential role in the establishment and maintenance of the carrier state."
Holyoak GR, et al., "Relationship between Onset of Puberty and Establishment of Persistent Infection with Equine Arteritis Virus in the Experimentally Infected Colt," (J Comp Pathol 1993; 109: 29)

"The relationship between stage of reproductive tract maturity and susceptibility to the experimental establishment of persistent infection with equine arteritis virus (EAV) was investigated in 21 prepubertal and 15 peripubertal colts. Five of six peripubertal colts inoculated intranasally remained infected in the reproductive tract from post-challenge day 28 to 93 and two of six from post-challenge day 120 to 180. No virus was detected in five of these animals killed on post-challenge day 210. Each of two peripubertal colts remained infected in the reproductive tract at post-challenge day 60 and one of nine was found to be persistently infected with EAV 15 months after challenge. These findings confirm that the virus can replicate in the reproductive tract of a significant proportion of colts for a variable period of time after clinical recovery in the absence of circulating concentrations of testosterone equivalent to those found in sexually mature stallions. Long-term persistent infection with EAV does not appear to occur in colts exposed to the virus before the onset of peripubertal development. We suggest that colts should be vaccinated at approximately 6 months of age, before peripubertal development but after the disappearance of maternally acquired antibodies."
There are a number of investigations that support my contention that testosterone adversely affects the immune system vis-à-vis the HIV. One contains this generality: "...sexually mature male vertebrates are often more susceptible to infection and carry higher parasite burdens in the field." (Int J Parasitol 1996; 26: 1009). Another investigation determined the following:

"CONCLUSIONS: Castration before soft-tissue trauma and hemorrhagic shock maintains normal immune function in male mice, but sham-castrated male mice show significant immunodepression. The maintenance of immune function by androgen deficiency does not seem to be related to changes in the release of corticosterone. We conclude that male sex steroids are involved in the immunodepression observed after trauma-hemorrhage. Thus, the use of testosterone-blocking agents following trauma-hemorrhage should prevent the depression of immune functions and decrease the susceptibility to sepsis under those conditions." (Arch Surg 1996; 131: 1186)

For sake of brevity, I have not gone in to detail regarding my explanation of how I think testosterone reduces the immune response. The next citation supports the negative effect of testosterone on the immune system, regarding malaria, and continues to say that the testosterone effect is not due to the classical explanation. My explanation does not rely on the "classical AR response."

"Our data suggest that testosterone suppresses the development of protective immunity against P. chabaudi malaria, and that this immunosuppressive effect of testosterone is not primarily mediated by the classical AR response." (J Endocrinol 1992; 135: 407)

Another investigation examined a specific phase of the immune response and found the same anti-immune function of testosterone. "These results suggest that the male sex hormone, testosterone, but not the female sex hormone has a role in the down-regulation of the systemic eosinophil responses of C57BL/6 mice to infection with B. pahangi." (Immunopharmacol 1992; 23: 75). You may know that tuberculosis, Mycobacterium tuberculosis, is more prevalent in blacks than whites, in a socioeconomically controlled study (New England J Med 1990; 322: 422). I explained this, then in 1990, as an example that testosterone adversely affects the immune system in humans, especially in blacks. In a study of mice exposed to Mycobacterium marinum, testosterone was found to increase susceptibility in males and females. This study carefully controlled for the presence of testosterone. "Although this ordering corresponded to the susceptibilities of both male and female mice to the organisms, much greater strain dependency was seen in males than in females. Castration caused an increase in the host resistance of males, but this effect was substantially reversed by continuous testosterone treatment. Testosterone also increased the susceptibility of female mice to this infection. These findings imply that the male sex hormone is involved in the lowered anti-M. marinum resistance of males." (Infect Immun 1991; 59: 4089).

Now, the data in the paragraph above, and citations regarding testosterone and the EAV in horses, all support negative effects of testosterone on differing types of infection in different mammals. Bearing in mind that I cited solid evidence that black males produce significantly more testosterone than white males and black females produce more testosterone than white females, it is my hypothesis that increased testosterone in blacks is why the HIV infects blacks more readily in the U.S.A. and much more so in Africa. For the very same reason, it also explains why blacks exhibit more tuberculosis, and other infections, than whites.

Copyright 1997, James Michael Howard, Fayetteville, Arkansas, U.S.A.

Dear Dr. Howard,

This concept is fascinating, do you have any cure for this elevated anount of testosterone? you think the hormone is braking down the immune system but how? and how can we lower the hormone level without suffering the consequences?
We need our hormones don't we?

Thanks,
Roshan

hi

your explanation is fascinating, but we also cannot think that human social factors are irrelevant here. Many Africans have more than one wife, and many more girlfriends on the side. This polygamy and very healthy appetite for sex and increase viral infection exponentialy.

i know, my answer is so simple but it has to be considered

HIV can only be defeated if we can fight its evolutionary advantage (copies itself wrong one too many times), in the end we must fight evolution

konstantinos

Has it occurred to you that many in our population may have been exposed to the HIV yet it only is successful in groups of high testosterone and / or low DHEA. For example, DHEA is known to be low in male homosexuals, overall, but there is overlap in levels. This means that some homosexuals have DHEA that is equal to heterosexual males. Therefore, I suggest there should be homosexual males who develop AIDS when exposed to the HIV (low DHEA), those who develop antibodies to the HIV but not AIDS (medium DHEA), and those who are not infected and do not even produce antibodies (high DHEA). These categories exist. That is, years ago a test was developed that determined there are homosexual males who practice "risk behaviors" who have been exposed to the HIV but do not even produce antibodies.
To see the chart, go to http://www.anthropogeny.com/AIDS%20and%20DHEA.htm and go to the third chart.)

I suggest this means that sufficient DHEA will stop the HIV before it even affects the body. I think a lot of people with sufficient DHEA are exposed to the HIV and other viruses and infectious agents but who fight these off before secondary (antibodies) are called into action. Not everybody who has sex with an infected person of some sort develop the infections.

Now, I know that abstinence and monogamy can simply stop the spread of infections. Wouldn't it be nice if everybody could control themselves like those who promote this method? However, they cannot and the consequences are becoming horrible. Now, I think DHEA will be useful in this fight and it is not patentable and cheap. There may be other methods to fight the HIV and I hope they work IF that is going to be the only way wealthy countries will try to attack this problem.

I agree with you, i am not trying to sound too conservative, but that is the reality of some African cultures. They are extremely promiscuous, but we are the ones making the drugs and the cures. I am all for great sex with lots of people, but safe sex is the best way to stay alive. Also knowing your partner's HIV status is helpful, somewhat awkward to ask on first meeting if its a one night stand!

safe sex is the way to go

I agree; safe sex is the way to go.

If one is older, one may wish to supplement with DHEA. I and my wife do. I and my wife never get the infections that periodically affect our population.

I have to agree that safe sex and a decrease in exchange of body fluids are excellent ways to avoid exposure to the article that causes infection: the virus.

The mentioned hypothesis is very intriguing. I would love to read more on this topic and the link of DHEA is also intriguing.

Thank you! I certainly agree that social and cultural beliefs and practices are almost infininitely more important in this disease than any hormonal differences for reasons that are so obvious.

It's distribution in all parts of the world is directly related to behavior more than any other factor--though other factors may have a minor role.

jim achmoody











quote=KONSTANTINOS]hi

your explanation is fascinating, but we also cannot think that human social factors are irrelevant here. Many Africans have more than one wife, and many more girlfriends on the side. This polygamy and very healthy appetite for sex and increase viral infection exponentialy.

i know, my answer is so simple but it has to be considered

HIV can only be defeated if we can fight its evolutionary advantage (copies itself wrong one too many times), in the end we must fight evolution

konstantinos[/quote]

"almost infininitely more important" ...Then it should be very, very easy for you to show this. ...go on, it should be easy...

Let me see if I have this correct: you're saying that testosterone/DHEA levels are more important than behavioral issues in determining the spread of AIDS? Even if you argue that there is not a simple statistical relationship between # of people infected with HIV in a given population vs. incidence of AIDS (not sure if this is part of your argument or not), it doesn't seem to take an epidemiologist to come to the conclusion that the best way to stop this disease is to stop viral transmission.
Of course, all the preaching by the religious right on the primacy of abstinence vs. birth control (e.g. condoms) is of no help whatsoever...

I am saying that the testosterone/DHEA ratio is important to the immune response and the same ratio is also directly involved in behavior. One is not more "important," both are involved. This ratio is directly involved in the immune response and the behavior. That is why these epidemics can expand so rapidly among groups that have a high testosterone to DHEA ratio. It is easy for someone who can control their behavior to also avoid infections. You see, after I developed this idea, it occurred to me that maybe there are people who may be exposed to HIV and respond so rapidly that even the antibody system is not called into effect. A long time ago, it was found that some homosexual males have been exposed to the HIV and not been infected and did not even exhibit antibodies. There are three groups of homosexual males who have been exposed to the HIV: one group does not get infected, does not even progress to antibody formation, and does not get sick, the next are exposed, form antibodies (the second defense) and do not get sick, and there is the group that get infected, form antibodies, and get sick and die. I attribute this to the relative levels of this ratio. If you want more detail: http://www.anthropogeny.com/AIDS%20and%20DHEA.htm .

Also, there is this publication, which the press and the AIDS people simply overlooked in 1991: "Although derived from independent samples and subject to different biases, these three survey methods yielded a consistent pattern of HIV-1 epidemiology on this campus, whereby the overall prevalence of infection was low and confined to members of high-risk groups, despite the common occurrence of behaviors that might facilitate sexual transmission of HIV-1 among many other students." (Am. J. Epidemiology 1991; 133: 2) It is not the behaviors that do it, it is something else. I think it is the testosterone to DHEA ratio or simply low DHEA.

You are correct; simply getting people to stop sexual activity with infected individuals will stop this. However, people do not understand the coupling of reduced impulse control and reduced immune response are tied together. Religion is a form of teaching impulse control. I think impulse control is declining because the number of people with increased testosterone to DHEA levels is increasing. Therefore, the traditional methods of teaching impulse control are not working anymore. When this happens, I think one is forced to go to plan B, some form of stopping infection during sex, which is difficult.

I think that this is a very good theory, but even so, if you sum the human behaviour with this DHEA theory with all the molecular mechanisms envolved in the virus infection we still cant awnser some trivial questions, like; why healthy people develop AIDS and people with depressed imune systems dont... In my point of view there is too much different symptoms related in this disease...Im not expert in virology, but still, I think that there is something wrong, maybe we didint find yet all the pieces of the puzzle.