Re: Why HIV is so Prevalent in Africa
From: James Michael Howard (jmhoward_at_anthropogeny.com)
Date: 10/12/04
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Date: Tue, 12 Oct 2004 13:18:08 GMT
This thread is so lengthy, I thought I would put my response first.
Anyone who is following this thread who has not read your remarks and
citations can read them on this post below my response. I hope you
find it interesting.
My explanation of AIDS involves more than testosterone. I emphasized
testosterone in my explanation of increased HIV / AIDS in blacks
because blacks produce more testosterone than whites and endogenous
testosterone and exogenous testosterone both increase infection rates
of other viruses in other mammals. The other aspect, the main one, of
my ideas about AIDS started in 1985. At that time I first suggested
low DHEA should increase vulnerability to the HIV (not called HIV at
the time). I think the loss of DHEA of AIDS actually causes the
symptoms of AIDS. The first reports of low DHEA in AIDS appeared in
1989. Since then, some papers have appeared which support low DHEA
and the symptoms of AIDS. Testosterone reduces DHEA availability;
testosterone reduces immune response. I put these ideas together to
explain why blacks exhibit more AIDS than whites. I omitted the DHEA
connection from my "Why HIV is so Prevalent in Africa," because I
thought the point was made without having to explain the underlying
mechanism of testosterone's effects on DHEA. (It was long enough as
is.)
Since you have brought the effects of age, etc. into this, I have to
access my hypothesis regarding DHEA and AIDS because these effects may
be due to DHEA availability. DHEA is low in early childhood, reaches
its peak around age twenty, then begins a decline to very low levels
in old age.
Testosterone should increase infection rates since testosterone
reduces immune response. Black men and women exhibit increased
infection rates. Once infected, I think men and women should differ
somewhat. Your first citation (Epidemiology. 1998 Nov;9(6):605-12)
says "Our analyses showed a SIMILAR disease progression in men and
women;" SIMILAR, but not identical. I think the progression rate
should be SIMILAR because the DHEA levels, while different between men
and women, are SIMILAR in men and women. (I think the lifespan is
determined by the availability of DHEA, directly affected by
testosterone levels. Men produce more testosterone than women so
men's lifespan is SIMILAR but slightly less.) DHEA declines in old
age, so your report says "a more rapid progression for older
subjects." It is my opinion that male homosexuality results from low
DHEA and it is known that, on average, DHEA is lower in male
homosexuals. Your report says: "a more rapid progression for older
subjects compared with younger ones and for homosexual men compared
with heterosexuals." Once infected, except for old people and
homosexual men of low DHEA, I would expect the progression rates to be
SIMILAR if one compares similar ages. This is what your report
states.
Your second citation (Ann Intern Med. 1990 Nov 15;113(10):733-9) may
also be illustrative of the connection of DHEA. First there is a
connection among the subjects, that is, needing blood components. If
I may, I suggest these are people who are, on the whole, ill. While I
do not want to debate this at length, a number of diseases and
disorders and post-surgery patients have been demonstrated to be low
DHEA. So, again, if I may, I suggest these people may have low DHEA.
Low DHEA is the key so the effects of testosterone may be moot in this
group. They may be vulnerable to infection because of low DHEA while
the "average" person with extra testosterone may be more vulnerable to
infection because of low DHEA caused by testosterone. This may be
like a "gate" that is opened by testosterone that the people of this
study have already opened. I suggest the authors of this study may
make my point when they said: "The rate of progression to AIDS within
the first 38 months after infection was SIMILAR to that reported for
homosexual men and hemophiliacs." I have already mentioned that, on
average, DHEA is low in homosexual men and DHEA is also low in
hemophiliacs. "Before HIV infection, men with hemophilia had
significantly lower plasma levels of DHEA-S than control men." (J Lab
Clin Med. 1996 Jun;127(6):545-52). (DHEA-S is the large, background
source in blood from which DHEA is converted.)
AIDS. 1992 Oct;6(10):1187-93 deals with women who are at least 50%
IVDU. I have long thought that drug addiction ultimately reduces
DHEA. A search of the literature will demonstrate that drugs of abuse
such as cocaine, morphine, etc. have now been connected with DHEA
levels. This area is only now beginning to appear but there are
indications that I may be correct. (Since some of your articles are
allowed to report SIMILAR findings, please allow me a little leeway
here to avoid lengthy time and debate regarding DHEA levels and drug
abuse.) Also, you point out that these women are being compared to
homosexual men who have "multiple other coinfections," and that "When
HIV-infected heterosexual women are compared with heterosexual men of
the same age, the difference in outcomes GENERALLY disappears." Well,
again, once the "gate" has been opened, the decline is SIMILAR because
men's and women's life spans are generally similar. I point out,
however, that your next citation, which you provided, says this:
"Co-infection with HCV and HTLV-II did not accelerate progression to
AIDS." Aren't these in the category of "multiple coinfections," yet
your citation says HCV and HTLV-II "did not accelerate progression to
AIDS." (Isn't it "interesting" that you say co-infection should
increase progression while a citation you provide says it does not.
It just does not seem "fair.")
J Acquir Immune Defic Syndr Hum Retrovirol. 1998;17 Suppl 1:S13-6
reports similar findings that may also be related to low DHEA. "Using
univariate analysis, more rapid progression was found for older
individuals than for younger individuals and for homosexual men
compared with those in other exposure categories." Again, older and
homosexual men, on average, produce less DHEA.
The report above also says: "Individuals with a history of acute HIV
disease were more likely to develop AIDS than other seroconverters."
To me, this indicates that individuals who have lost enough DHEA to
exhibit "acute HIV disease" are already low in DHEA and will progress,
that is, lose DHEA, faster. I have said "on average" a couple of
times regarding low DHEA in homosexual men on purpose. You see, my
explanation of AIDS is that it is low DHEA that increases
vulnerability to infection and loss of DHEA that results in the
symptoms of AIDS. When the DHEA reaches too low levels, I suggest
death occurs as is the same of old people. I have suggested,
elsewhere, that AIDS is "accelerated aging." If I am correct, then
one should see homosexual men who are infected and die from AIDS: low
DHEA and loss of DHEA; one should see homosexual men who are infected,
that is, show antibodies, but do not die from AIDS: medium DHEA; and
homosexual men who are proven to have been infected but do not develop
antibodies and do not show ill effects: high DHEA. I suggest many
individuals of high DHEA have been exposed to DHEA but do not even
exhibit an antibody response because the antibody response is a
secondary level of protection from the HIV.
Well, I hope you have found this "interesting." I may have avoided
having to take your time, and any readers' time, if I had included the
connection of low DHEA with testosterone in my "Why HIV is so
Prevalent in Africa," but I doubt it. I had intended reduce the need
to support another hypothesis about testosterone and infection with
another regarding DHEA and infection to keep the article brief.
On 11 Oct 2004 19:55:38 -0700, sbharris@ix.netcom.com (Steve Harris
sbharris@ROMAN9.netcom.com) wrote:
>James Michael Howard <jmhoward@anthropogeny.com> wrote in message news:<hbokm0dnvl4t6u1k2r9ls28o53k2vuhkdl@4ax.com>...
>> On 10 Oct 2004 17:58:06 -0700, sbharris@ix.netcom.com (Steve Harris
>> sbharris@ROMAN9.netcom.com) wrote:
>>
>> >James Michael Howard <jmhoward@anthropogeny.com> wrote in message news:<bevim0hv67g7039t4qh5pe944s51htm1g7@4ax.com>...
>> >> Why HIV is so Prevalent in Africa:
>> >> http://www.anthropogeny.com/Why%20HIV%20is%20so%20Prevalent%20in%20Africa.htm
>> >
>> >
>> >COMMENT:
>> >
>> >One problem with your hypothesis is that it runs up severely into some
>> >nasty facts. We know testosterone cannot be a very important factor
>> >in development of HIV infection into AIDS, because risk of people who
>> >seroconverted to HIV after transfusions of tainted blood (in the mid
>> >1980's before the HIV test was available to screen the blood supply)
>> >have been examined. There's a big age effect in such data (the older
>> >the person, the sooner they develop AIDS after HIV seroconversion from
>> >a transfusion), but there is no sex effect. Women take about the same
>> >average time (10 years) to develop transfusion-related AIDS as do men.
>> >
>>
>> Thanks, Steve. Please provide citations to support your remarks. I
>> had a lot of trouble finding support for you remarks. I need this in
>> order to better respond.
>
>COMMENT:
>
>This should be interesting.
>
>There are many such papers. Here are 4 off the top. You can also look
>at any good textbook of AIDS, and I suggest you do so..
>
>
>1. Epidemiology. 1998 Nov;9(6):605-12.
>
>Comment in:
> Epidemiology. 1998 Nov;9(6):590-3.
>
>Effect of gender, age, transmission category, and antiretroviral
>therapy on the
>progression of human immunodeficiency virus infection using multistate
>Markov
>models. Groupe d'Epidémiologie Clinique du SIDA en Aquitaine.
>
>Alioum A, Leroy V, Commenges D, Dabis F, Salamon R.
>
>INSERM U330, Universite Victor Segalen, Bordeaux, France.
>
>This article illustrates the use of time-homogeneous Markov models
>with
>covariates to estimate the AIDS incubation period distribution from
>prevalent
>cohorts and to evaluate the effect of factors such as gender, age,
>human
>immunodeficiency virus (HIV) transmission category, and antiretroviral
>therapy
>on disease progression. We applied this methodology to the analysis of
>data from
>a cohort of 3,027 patients enrolled from a hospital-based surveillance
>system of
>HIV infection in the Bordeaux University Hospital and four secondary
>public
>hospitals in southwestern France. A total of 998 individuals (33%)
>progressed to
>AIDS during a median follow-up period of 34 months. Based on a
>progressive
>three-state Markov model, the estimated mean and median incubation
>periods were
>9.1 years [95% confidence interval (CI) = 8.7-9.6] and 7.5 years (95%
>CI =
>7.2-7.9), respectively. Our analyses showed a similar disease
>progression in men
>and women {please note, Mr. Howard]; we observed a more rapid
>progression for older subjects compared with
>younger ones and for homosexual men compared with heterosexuals,
>intravenous
>drug users, and transfusion recipients, who had similar disease
>progression
>rates after adjusting for age. The use of antiretroviral therapy
>appeared to
>slow disease progression. Moreover, the results indicated that a
>combination
>therapy of zidovudine with another antiretroviral drug may be more
>efficient
>than zidovudine monotherapy.
>
>PMID: 9799168 [PubMed - indexed for MEDLINE]
>
>
>
>2. Ann Intern Med. 1990 Nov 15;113(10):733-9.
>
>Comment in:
> Ann Intern Med. 1990 Nov 15;113(10):729-30.
>
>Infection with human immunodeficiency virus type 1 (HIV-1) among
>recipients of
>antibody-positive blood donations.
>
>Donegan E, Stuart M, Niland JC, Sacks HS, Azen SP, Dietrich SL,
>Faucett C,
>Fletcher MA, Kleinman SH, Operskalski EA.
>
>University of California, San Francisco.
>
>OBJECTIVE: To assess the incidence of human immunodeficiency virus
>type 1(HIV-1)
>transmission by antibody (anti-HIV-1)-positive blood components, and
>to
>determine the immunologic and clinical course in HIV-1-infected
>recipients.
>DESIGN AND SUBJECTS: We retrospectively tested approximately 200,000
>donor blood
>component specimens stored in late 1984 and 1985 for anti-HIV-1, and
>we
>contacted recipients of positive specimens to determine their
>serologic status.
>They were compared with both recipients of HIV-1-negative transfusions
>and
>healthy (untransfused) controls. Subjects were seen at 3- to 6-month
>intervals
>for up to 4 years for clinical and immunologic evaluations.
>MEASUREMENTS AND
>MAIN RESULTS: Of 133 recipients, 9 had other possible exposures.
>Excluding these
>cases, 111 of 124 (89.5%) were anti-HIV-1-positive (95% CI, 84.1% to
>94.5%). The
>recipient's sex, age, underlying condition, and type of component did
>not
>influence infection rates [Please note, Mr. Howard]. The cumulative
>risk for developing the acquired
>immunodeficiency syndrome (AIDS) within 38 months after transfusion
>was 13% (CI,
>7.5% to 21.6%). At 36 +/- 3 months after the index transfusion,
>seropositive
>recipients had lower counts of CD2+CDw26+, CD4+, CD4+CD29+, and
>CD4+CD45RA+subsets and more CD8+I2+ lymphocytes than did recipients of
>anti-HIV-1-negative transfusions. The CD4+ and CD2+CDw26+subsets
>changed the
>most rapidly. The absolute CD8+ count remained normal. CONCLUSIONS:
>Transfusion
>of anti-HIV-1-positive blood infected 90% of recipients. The rate of
>progression
>to AIDS within the first 38 months after infection was similar to that
>reported
>for homosexual men and hemophiliacs. Although most lymphocyte subset
>counts
>changed over time, CD8+ counts were constant.
>
>PMID: 2240875 [PubMed - indexed for MEDLINE]
>
>
>3. AIDS. 1992 Oct;6(10):1187-93.
>
>Women and HIV infection: a cohort study of 483 HIV-infected women in
>Bordeaux,
>France, 1985-1991. The Groupe d'Epidémiologie Clinique du SIDA en
>Aquitaine.
>
>Morlat P, Parneix P, Douard D, Lacoste D, Dupon M, Chene G, Pellegrin
>JL,
>Ragnaud JM, Dabis F.
>
>Centre Hospitalier Regional et Universitaire (CHRU) of Bordeaux,
>France.
>
>OBJECTIVES: To study the epidemiological trends, clinical patterns,
>evolution
>and prognosis of HIV infection in women. DESIGN: Cohort study of 1816
>HIV-infected patients. RESULTS: Up to 1 January 1991, 483 (26.6%) of
>the
>patients reported to the Groupe d'Epidemiologie Clinique du SIDA en
>Aquitaine
>surveillance system were women. The male-to-female ratio has decreased
>progressively (3.4:1 in 1985; 2.7:1 in 1990) over time. Fifty per cent
>of
>HIV-infected women are or have been intravenous drug users (IVDU). The
>proportion of heterosexually acquired HIV infection increased from
>11.6 to 34.6%
>over the last 5 years; 46.9% of the women infected through
>heterosexual
>intercourse reported sexual contacts with male IVDU. Excluding
>Kaposi's sarcoma,
>no significant difference was observed between men and women in the
>overall
>distribution of AIDS-defining events. The observed trend of a slower
>progression
>to AIDS in women, compared with men, disappeared when controlling for
>prognostic
>variables. However, female sex significantly enhanced survival after
>AIDS
>diagnosis in multivariate analysis (relative risk, 2.7; 95% confidence
>interval,
>1.1-6.2). CONCLUSION: Early diagnosis of HIV infection in female
>patients and
>prevention of HIV infection among women is now a priority for public
>health
>interventions, both in industrialized and in developing countries.
>
>PMID: 1466851 [PubMed - indexed for MEDLINE]
>
>
>Comment: Note that the enhanced survival of women here after AIDS
>appears, is by comparison to homosexual men. This is not a fair
>comparison since homosexual men are known to have multiple other
>coinfections. When HIV-infected heterosexual women are compared with
>**heterosexual men of the same age,** the difference in outcomes
>generally disappears.
>
>
>
>4. J Acquir Immune Defic Syndr Hum Retrovirol. 1998;17 Suppl 1:S13-6.
>
>Determinants of progression to AIDS in HIV-infected individuals: an
>update from
>the Italian Seroconversion Study.
>
>Rezza G.
>
>National AIDS Unit, Centro Operativo AIDS, Istituto Superiore di
>Sanita, Rome,
>Italy.
>
>The Italian Seroconversion Study (ISS) involves 16 major HIV-treatment
>centers
>across Italy and about 1,200 individuals. These individuals were
>HIV-negative
>less than 2 years before the first positive test and seroconverted
>between 1980
>and 1994. The majority were infected through i.v. drug use (56%),
>male-to-male
>sex (25%), and heterosexual contact (7%). For each end point, crude
>and adjusted
>relative hazards were calculated using standard survival techniques
>such as
>Kaplan-Meier curves, log-rank test, and Cox proportional hazards
>regression
>models. Autoregression models were used to describe CD4 cell
>reductions.
>Objectives were as follows: to estimate HIV disease progression rates;
>to assess
>whether there are differences in the rate of development of severe
>immunosuppression, AIDS, and death according to age, gender, and
>exposure
>category; to identify co-factors and predictors of disease
>progression; and to
>evaluate the clinic-based population "effect" of antiretroviral
>treatment. The
>risk for developing AIDS among individuals in the ISS cohort was less
>than 50%
>by 10 years after HIV seroconversion. Using univariate analysis, more
>rapid
>progression was found for older individuals than for younger
>individuals and for
>homosexual men compared with those in other exposure categories. No
>difference
>between men and women was observed. [Please note, Mr. Howard] After
>adjusting for age, differences among
>exposure groups disappeared. Individuals with a history of acute HIV
>disease
>were more likely to develop AIDS than other seroconverters.
>Co-infection with
>HCV and HTLV-II did not accelerate progression to AIDS. The cumulative
>incidence
>of receiving pre-AIDS therapy within 7 years of seroconversion was
>49.2% (95% CI
>45.3-53.0). The relative hazards of developing AIDS in patients who
>started
>treatment with zidovudine (AZT) monotherapy was 0.57 (0.36-0.91) and
>0.92
>(0.64-1.33) within the first year and after 1 year from AZT
>initiation,
>respectively. The effect was greater among homosexual men than among
>i.v. drug
>users. In conclusion, incident cohort studies may provide accurate
>information
>on incubation time and co-factors for disease progression.
>Observational studies
>may also provide useful information about the effect of treatment at
>the
>community level, which may complement the results of clinical trials.
>
>Publication Types:
> Multicenter Study
>
>PMID: 9586645 [PubMed - indexed for MEDLINE]
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