Re: Re: Re: Re: Re: Re: Yet More on Oxidation – the primary cause for AIDS and “HIV” 4 April 2005
Previous Rapid Response Next Rapid Response Top
Christopher Tyler,
n/a
84102

Send response to journal:
Re: Re: Re: Re: Re: Re: Re: Yet More on Oxidation – the primary cause for AIDS and “HIV”

Mr. Bennett wrote:

"The issue of poppers in KS has been addressed several times. Ascher et al found no correlation between popper use and risk of AIDS, independant of HIV infection. [3]."

The Ascher study does anything but prove that 'HIV' is the sole cause of these mens' illnesses. They claimed that "when controlled for HIV serostatus, there is no overall effect of drug use on AIDS..."

However, how could they have known this when all 'HIV' positives were gay men, and according to Table 2, 100% of these gay men were also either 'heavy' or 'light' nitrite users (in addition to an unreported percentage who also used other illicit recreation drugs such as cocain and amphetamines). Put succinctly, they didn't have proper controls.

Further confounding the study results was the fact that many of these men were on AZT which, when coupled with the higher dose regimen of the time, would have been a most definitive factor in negatively impacting their health (please refer to the Concorde Trials for the deliterious effects of AZT, Appendix 1).

Aside from not having actual drug-free 'HIV' positive controls, they also contradicted themselves by having found "heavy" drug users had twice the rate of AIDS and particularly of KS than "light" users (Table 2).

For a more complete analysis of the Ascher paper and it's sister study (Schechter, et. al. Vancouver) please visit:
http://www.virusmyth.net/aids/data/pdaifo93.htm

Specifically, read section 3 (Failure to Identify Drug-Free AIDS, the Absolute Argument against the Drug-AIDS Hypothesis).

Also, please visit the link below to see further correlation between drug abuse and AIDS:
http://www.virusmyth.net/aids/data/pddrtab5.htm

Would Mr. Bennett please provide studies which demonstrate that in the ABSENCE of illicit drug usage; in the ABSENCE of malnutrition; in the ABSENCE of antiretroviral usage, so-called HIV positive individuals develop 'AIDS'. Put another way, would Mr. Bennett please show that otherwise healthy individuals who are 'HIV' positive (white heterosexual females for instance) develop 'AIDS'.

For instance, could Mr. Bennett please explain how Christine Maggiore and Kim Bannon are not dead from AIDS and are still healthy even though both tested 'positive' in 1992? Both of these females fit the above categorization. (Ms. Bannon's doctor even said her WB results were 'classic' for 'HIV' infection in 1992). How is it possible these women 13 years on have not gotten sick and developed so-called AIDS?

The studies Mr. Bennett supplied draw on cohorts of individuals replete with confounding factors, both factors which confound their health and confound the antibody tests used to 'diagnose' them.

For instance, his reference 7 (Goedert et al. Science. 1986 Feb 28;231(4741):992-5. "Three-year incidence of AIDS in five cohorts of HTLV-III-infected risk group members.") states, "The incidence of the acquired immune deficiency syndrome (AIDS) among persons infected with human T-lymphotropic virus type III (HTLV-III) was evaluated prospectively among 725 persons who were at high risk of AIDS and had enrolled before October 1982 in cohort studies of homosexual men, parenteral drug users, and hemophiliacs."

and;

"By actuarial survival calculations, the 3-year incidence of AIDS among all HTLV-III seropositive subjects was 34.2 percent in the cohort of homosexual men in Manhattan... and 14.9 percent... in the four other cohorts."

Peter Duesberg has deftly shown that homosexual men who are said to be 'HIV' positive and develop AIDS are almost 100% likely to have used illicit drugs in conjunction with repeated exposure to many std's and their treatments.

In the same study by Goedert et al., they state, '...risk of AIDS development in different populations may also depend on the presence of as yet unidentified cofactors."

Remember what I said about denial in the medical community?

Given that the Manhattan men were at twice the risk of developing 'AIDS' as the other risk groups; and given that Peter Duesberg has shown the groups of men these studies draw upon were 100% saturated with 'unidentified cofactors' (euphamism for stds, their treatments, repeated rectal semen exposure, illicit drug abuse--all of which negatively impact the redox state) demonstrates the dose dependent manner in which these 'unidentified cofactors' increased their risk of getting sick and dying. The Ascher San Francisco study as mentioned above demonstrated this.

In his book "AIDS The failure of contemporary science: How a virus that never was deceived the world", Neville Hodgkinson lists one gay man's repeated STD infections, "Non-specific urethritis, hepatitis A, more NSU and gonorrhoea, amoebas [intestinal parasites]-and hepatitis B, more NSU and gonorrhoea, more amoebas, shigella, non-A, non-B hepatitis, giardia, anal fissures, syphilis, more gonorrhoea [penile, anal and oral], gonorrhoea, shigella twice, more amoebas, herpes simplex types I and II; venereal warts, salmonella; chlamydia; cytomegalovirus (CMV); Epstein-Barr virus (EBV); mononucleosis and cryptosporidiosis".

Indeed, Callen reports in his book, "Surviving AIDS", his over 3000 sexual contacts and extensive drug use before he adopted a monogamous lifestyle (Callen, 1990).

In Mr. Bennett's reference 7 (Goedert et al.), it's not the least bit surprising that many of these men were showing up positive, given that:

  • historically the ELISA's have been terribly non-specific (1);
  • Up until 1987, merely having a p24 or p41 was sufficient for a 'positive' Western Blot diagnosis;
  • the cohort of men from New York were immunological battlegrounds (hypergammaglobulinemic), meaning they had antibodies to all manner of agents such as (but not limited to) sperm, fungi, viruses, parasites in addition to having antibodies to 'self' such as collagen and polymerised (oxidized) actin—all of which are known to cross-react to the 'HIV' antibody tests;
  • the cohort of men from New York as utilized by the Goebert study were likely to have high levels of circulating immune complex(2) which have been associated with a positive 'HIV' antibody test.

It's therefore not the least bit surprising that these men had antibodies reactive to the 'HIV' antibody tests. Prior to the advent of 'HIV' and its accreditation as the causal factor in these men's health problems, it had already been established that drug abusers often had false positive tests, including antibody tests (in addition to health problems that mimmic 'HIV infection'– see appendix 2). In 1986 Jaffe and his colleagues wrote, "It is also recognised that asymptomatic parenteral drug abusers often have hypergammaglobulinemia, high titers of immune complexes, a high prevalence of positive tests for rheumatoid, and high rates of false positivity on a number of routine laboratory tests... On the basis of our positive Western blot data, it appears possible that parenteral drug abusers may have been exposed to HTLV-III or a related virus as early as 1971. An alternative but equally viable explanation is that the HTLV-III seropositivity detected in these specimens represents false positive or nonspecific reactions" (Jaffe et al. 1986).

It's also not the least bit surprising that these tests would react to individuals with the greatest propensity to develop illnesses and die, especially when one considers Gallo designed these tests from the sera of sick gay men. Indeed, Darby et al.,(3) showed that 'HIV infection' (that is, a positive antibody test) predicted mortality from not only AIDS defining illnesses but also from non-AIDS defining illnesses in haemophiliacs (of the 403 deaths in seropositive individuals, 235 died from "AIDS, HIV, etc"., while 168 died from causes other than AIDS.)

Put simply, Mr. Bennett's reference 7, as an example, is anything but proof that so-called HIV was the cause of these men's illness. The antibody reactions in these men were non-specific reactions.


Mr. Bennet wrote:

'It is only after this point that CD4 T cells decline."

A prospective study of male homosexuals using psychoactive and sexual stimulants demonstrated that their T-cells may decline prior to infection with 'HIV'. For example, the T-cells of 37 gay men from San Francisco declined steadily prior to HIV infection for 1.5 years from over 1200 to below 800 per µl (Lang et al., 1989).

In some case they had fewer than 500 T-cells 1.5 years before seroconversion (Lang et al., 1987).

Other studies of the same cohort of homosexual men from San Francisco described extensive use of recreational drugs including nitrites (Darrow et al., 1987; Moss, 1987; Ascher et al., 1993; Duesberg, 1993d; Ellison, Downey and Duesberg, 1995). Likewise 33 HIV-free male homosexuals from Vancouver, had "acquired" immunodeficiency prior to HIV infection (Marion et al., 1989). While this study did not mention drug use, other articles by the authors reported that all men of this cohort had used nitrites, cocaine and amphetamines (Archibald et al., 1992; Duesberg, 1993f; Schechter et al., 1993c).

In 1994, a study of IV drug users in New York (Des Jarlais et al., 1993) showed that "The relative risk for seroconversion among subjects with one or more CD4 count <500 cells/uL compared with HIV-negative subjects with all counts >500 cells/uL was 4.53".

A similar study in Italy (Nicolosi et al., 1990) showed that "low number of T4 cells was the highest risk factor for HIV infection", that is, decrease in T4 cells is a risk factor for seroconversion and not vice versa.


Mr. Bennett wrote:

"It also fails to explain why HIV antibodies (which correlate with virus culture and PCR - standards far in excess of those expected of other pathogens) correlate with a massively increased risk of opportunistic infections independantly of other factors."

Would Mr. Bennet please define what a positive Wester Blot is. So far, no one seems to agree on what that is.

Is a p24, p32, and p41 positive?
How about p41 and gp120?
How about p24, p68, p41, and gp120?
How about p41, gp120, and gp160?
How about p18, p24, p32, p53 and p68?
How about p24 by itself?
How about p18, p24, p55 and gp120?

Then, would Mr. Bennett please look over this chart and tell us which of the viral loads presented (collumn 1, 2, or 3) would be the correct measure to correlate with the correct Western Blot pattern(s) from above.

With regard to the above discussed Ascher study, its sister study (Schechter et al., Vancouver) reported in 1991 that 33 out of 158 (17%) of 'Western blot-confirmed' (whatever that means), antibody-positives in their Vancouver cohort were 'HIV-free', when the unsuitable 'gold standard' of HIV DNA (PCR) testing was used (4). Two of these 33 had AIDS, the remainder had various degrees of immunodeficiency and lymphadenopathy. The report also cites further studies documenting that 14 to 17% of antibody-positive homosexuals are 'HIV-provirus' free.

M Burgard et al., of the French Collaborative Study Group wrote of newborn infants, 'Of the 181 infants, 3 died of HIV infection and 37 were seropositive after the age of 18 months. Viral cultures at birth were positive in 19 of the 40 infected infants and in none of the uninfected infants, yielding a sensitivity of 48 percent... By the age of three months, 30 of the 40 infants (75 percent) had positive cultures... The sensitivity of testing for p24 antigen at birth was only 18 percent... Viral culture at birth can correctly identify about half of newborns with HIV infection.'(5)

In 2000, the CDC wrote, "HIV nucleic acid (DNA or RNA) detection tests are the virologic methods of choice to exclude infection in children aged less than 18 months. Although HIV culture can be used for this purpose, it is more complex and expensive to perform and is less well standardized than nucleic acid detection tests"(6)

Question. If 'nucleic acid (DNA or RNA) detection tests are the virologic methods of choice to exclude infection in children aged less than 18 months', why is it not allowed for diagnosis in adults?

With regard to 'virus culture' this is often nothing more than another antibody reaction or indirect detection of reverse transcription activity. It's scientifically invalid to use one antibody reaction as a gold standard for another one. According to Philip Mortimer and his colleagues from the UK Public Health Laboratory Service: "Experience has shown that neither HIV culture nor tests for p24 antigen are of much value in diagnostic testing. They may be insensitive and/or non-specific"


Mr. Bennett wrote:

"It should not be forgotten that HIV is itself an infection"

I didn't note a reference to this assertion. Would you please provide references that antibodies reacting to the 'HIV' test are induced specifically in response to 'HIV'. This would require a gold standard, one which so far no one, not even Abbot Laboratories have known about.


1. Burke, D.S., et al. NEJM 319, 961-964 (1988)

2. http://www.virusmyth.net/aids/data/jsochapter29.htm

3. Mortality before and after HIV infection in the complete UK population of haemophiliacs. UK Haemophilia Centre Directors' Organisation., Nature. 1995 Sep 7;377(6544):79-82.

4. Schechter, M.T., Neumann, P.W., Weaver, M.S., et al.: Low HIV-1 proviral DNA burden detected by negative polymerase chain reaction in seropositive individuals correlates with slower disease progression. AIDS 5, 373-379 (1991).

5. http://content.nejm.org/cgi/content/abstract/327/17/1192

6. CDC. (1999). Guidelines for national human immunodeficiency virus case surveillance, including monitoring for human immunodeficiency virus infection and acquired immunodeficiency syndrome. Morbidityand Mortality Weekly Reports 48:1-27, 29-31. www.cdc.gov/epo/mmwr/preview/mmwrhtml/rr4813a2.htm


Appendix 1

“participants of open-label ZDV [AZT] still had four to five times the incidence of ARC/AIDS/death of participants on blinded therapy [of which approximately half were on AZT and half on placebo]...The unadjusted hazard of ARC/AIDS/death was 4.6 times higher for participants [in the deferred group] who had received ZDV...after adjustment for latest CD4 this became 1.6...There was a suggestion of a benefit in terms of [slower] progression to ARC, AIDS or death [with AZT], no effect on progression to AIDS or death, and a suggestion of an increase in mortality. ”
White IR et al. Impact of treatment changes on the interpretation of the Concorde trial. AIDS. 1997;11:999-1006.

“Extended follow-up of patients in one [AZT] trial, the Concorde study, has shown a significantly increased risk of death among the patients treated early...where is the evidence that for a patient with a CD4 count of 450 cells per cubic millimeter and a low plasma viral level, it would not be better to wait before initiating therapy?...In 1990...a patient with a CD4 count of 450 cells per cubic millimeter would have been advised to start monotherapy with zidovudine. We now tell such a patient that, in fact, follow-up data for up to 4.5 years since that time have shown no survival benefit ”
Phillips AN, Smith GD et al. Viral load and combination therapy for Human Immunodeficiency Virus. N Engl J Med. 1997 Mar 27;336(13):958-9; author reply 960.

“A total of 172 (96 Imm, 76 Def) participants died [169 who had taken some AZT, 3 who had only taken placebo]...The results of Concorde do not encourage the early use of zidovudine in symptom-free HIV-infected adults. They also call into question the uncritical use of CD4 cell counts as a surrogate endpoint for assessment of benefit from long-term antiretroviral therapy...Representatives of the Wellcome Foundation [Glaxo Wellcome manufactures AZT] who were also members of the Coordinating Committee have declined to endorse this report.”
Concorde Coordinating Committee. Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and deferred zidovudine in symptom-free HIV infection. Lancet. 1994 Apr 9;343(8902):871-81.

Appendix 2

Before the 'HIV' era, It was known that IV drug abusers suffered from illnesses and conditions that 'mimmic HIV'. For instance Dr. R. P. Brettle, MD (Univerisity of Edinburgh, Scottland), speaking of IV drug users in Scottland says:

'The extent of the injection drug use (IDU) related HIV epidemic in Edinburgh requires consideration of the clinical features of IDU as well as those of HIV since each may mimic the other. As an example, lymphadenopathy is associated with both HIV and with the injecting of foreign materials... Diarrhoea, a common presentation of early symptomatic HIV (CDC stage IVA) is unfortunately a common problem with opiate withdrawal. A history of diarrhoea for longer than 1 month may be elicited via direct questioning and suggest a possible diagnosis of CDC stage IVA. Such as history would also require a search for specific pathogens such as cryptosporidium which are seen in AIDS. However early morning diarrhoea is common for those on methadone and is simply a symptom of early opiate withdrawal. Weight loss and sweating are both key symptoms of constitutional disease (CDC stage IVA) as well as mycobacterial infections, yet both are associated with heavy opiate use or the use of stimulants (amphetamines or cocaine).
http://www.link.med.ed.ac.uk/RIDU/Clidu.htm

"Maternal drug abuse is associated with a shortergestational age and a low birthweight, and most of our HIV-positive mothers for whom a full history is available abused intravenous drugs during pregnancy: this, rather than HIV infection, may be mainly responsible forpreterm delivery and the low birthweight"
Italian Multicenter Study

Competing interests: None declared