More on Oxidation – the primary cause for AIDS and “HIV” 1 February 2005
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Eleni Papadopulos-Eleopulos,
Biophysicist
Department of Medical Physics, Royal Perth Hospital, Western Australia, 6001,
Valendar F Turner, John Papadimitriou, Barry Page, David Causer, Helman Alfonso, Sam Mhlongo, Todd Miller, Christian Fiala

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Re: More on Oxidation – the primary cause for AIDS and “HIV”

More on Oxidation – the primary cause for AIDS and “HIV”

 

In his rapid response, “Re: Oxidation – the primary cause for AIDS and “HIV”” (22 January 2005), Nicholas Bennett wrote: “In response to the Perth Group:

I find no evidence that suggests that semen, nitrite inhalants, or factor VIII are "oxidative".   I think Mr Whitehead gave some evidence that opiods can affect cellular redox but this does not mean that they are oxidiative in the chemical sense.”  Malnutrition itself may not lead to "oxidation" (whatever that means - spontaneous combustion?) but it will of course lead to reduced intake of antioxidant nutrients which will perhaps lead to a reduced ability to deal with other stressors which may themselves be the cause of altered cellular redox.”

These statements yet again indicate that he may not be aware what oxidation is. (Oxidation is NOT “spontaneous combustion”).   In view of this, it is amazing that Nicholas Bennett has been repeatedly slating our oxidative theory.     All he has to do in order to find that semen, nitrites and factor VIII are strong oxidising agents is to read: “Reappraisal of AIDS – Is the Oxidation Induced by the Risk Factors the Primary Cause?”(1).

If something “affect cellular redox” and yet not be “oxidative in the chemical sense” then in what sense are they oxidative?   

The statement regarding malnutrition is rather contradictory.   He admits that malnutrition leads to a “reduced intake of antioxidants.    Doesn’t it follow that this will lead to oxidation?

Would Nicholas Bennett explain what he means by the term “stressors” and why they and not the lack of antioxidants are the cause of the oxidation?

 

Nicholas Bennett wrote: “I see no evidence therefore that AIDS patients are exposed to cellular oxidizing agents above and beyond non-AIDS patients.”

If there is no evidence that AIDS patients are exposed to cellular oxidising agents above and beyond non-AIDS patients then what is the cause of their oxidative status?

 

Nicholas Bennett wrote: “The main predictions of the HIV/AIDS theory are that:

HIV serology should precede AIDS.”

We have always maintained that a positive antibody test predicts the presence of future development of pathology including the diseases which are said to indicate AIDS.   The question is “Do these antibody tests prove “HIV” infection?”  Neither Nicholas Bennett nor Peter Flegg nor Brian Foley nor anybody else has given any evidence to support “HIV” infection.

In his latest effort to justify the “HIV” Western Blot test, (“HIV tests”, 26 January 2005) all Nicholas Bennett could give answering Rob McGregor (Re: Re: Oxidation – the primary cause for AIDS and “HIV””, 25 January 2005) was: “The differences in Western Blot criteria again boil down to differences in the test kits used. Each kit is developed differently - some using recombinant proteins, some using virus preps, some using peptides. It makes sense that depending on the specific antigen being presented and the mode of presentation, sensitivity and specificity for individual bands will vary. This is why each kit includes appropriate interpretation instructions, again based upon comparisons with standardised panels.”

It is true that the test kits may contain different antigens.   However, it is also true, and surely Nicholas Bennett is aware of this, that one and the same kit is used in different countries and different laboratories with different criteria of interpretation of the results based upon different “standardised panels”.   Furthermore, these “standardised panels” and the criteria for a positive test have been introduced arbitrarily.   Surely Nicholas Bennett is aware that the specificity of the “HIV” antibody tests can be determined only by comparing the results of the antibody tests with the presence or absence of “HIV”.  (The presence or absence of “HIV” must be determined by a method which does not involve antibody-antigen reactions, namely “HIV” isolation).

 

Nicholas Bennett wrote: “HIV serology should predict HIV detection via other means (e.g. culture, PCR, antigen testing).”

In the antibody tests, the “HIV” proteins are given and are reacted with sera containing antibodies.   When a reaction takes place, the reacting antibodies are said to be “HIV”.

In “culture” and “antigen testing”, the “HIV” antibodies are given and are reacted with either the culture contents or with antigens.   If a reaction takes place, then it is claimed proof for “HIV isolation” or detecting of “HIV” proteins.  (See the very often cited papers by David Ho or Brooks Jackson

Since it is the same reaction involved in the three tests, it is likely that some correlation is found between them.

Would Nicholas Bennett please give us a few references in which the specificity of the PCR for “HIV” has been proven.

 

Nicholas Bennett wrote: “Pharmacological intervention against the virus should inhibit the viral replication in vitro and in vivo, and result in restoration of the immune dysfunction seen in AIDS and pre-AIDS complex patients.

Would Nicholas Bennett please give us a few references where it has been shown that “viral load” means “HIV” infection and that a decreased “viral load” means inhibition of “HIV” replication.

 

Nicholas Bennett wrote: “HIV serology should, obviously, appear to be transmissible and associate with the individuals and risk groups associated with AIDS.”

The main mode of “HIV” transmission is said to be sexual and the main risk groups in the developed countries to be gay men.   Let us once again remind Nicholas Bennett that bi-directional transmission is required for an agent to be sexually transmitted.  In a previous rapid response we drew attention to the following facts.    In 1984, Robert Gallo and his colleagues wrote “Of eight different sex acts, seropositivity correlated only with receptive anal intercourse…and with manual stimulation of the subject’s rectum (receptive “fisting”)…and was inversely correlated with insertive anal intercourse.”2  Two years later they confirmed their 1984 findings: “In this analysis, only receptive rectal intercourse, douching, rectal bleeding…were significant predictors (p<.05) of anti-HTLV-III positivity…We found no evidence that other forms of sexual activity contributed to the risk.”3  In a 1994 review of all the major studies conducted in gay men including the longest, largest, best-designed and executed published study of gay men anywhere in the world, the MultiCenter AIDS Cohort Study, the authors concluded: “(1) unprotected anogenital receptive intercourse poses the highest risk for the sexual acquisition of HIV-1 infection;  (2) anogenital insertive intercourse poses the highest risk for the sexual transmission of HIV-1 infection;  (3) there is mounting epidemiologic evidence for a small risk attached to orogenital receptive sex,…(4) sexual practices involving the rectum and the presence of (ulcerative) STD facilitate the acquisition of HIV-1;  (5) no or no consistent risk for the acquisition of HIV-1 infection has been reported regarding other sexual practices such as anogenital insertive intercourse and oroanal sex…”.

Since the main and absolutely necessary property of sexually transmitted agents is bidirectionality, that is, transmission from the passive to the active partner and vice versa, this means “HIV” cannot be sexually transmitted.   In other words, “HIV serology” like pregnancy, is sexually acquired but is not sexually transmitted.

 

Nicholas Bennett wrote: “All of these are true and have been discussed here before” - in order for the Perth Group to maintain their oxidative stress theory they have had to concoct terribly convoluted explanations for the serology and culture methods, when Occam's Razor dictates that the simplest explanation is most usually the correct one.

If anything is “convoluted” it is their way of attempting to justify “serology” (whatever he means by it) with “culture methods” (whatever he  means by it) and “PCR” and vice versa without resorting to basic scientific principles to show that at least one of them proves “HIV” infection.

 

Nicholas Bennett wrote: “One ommission made in the Oxidative theory of AIDS is that those with oxidative stress but without HIV should get AIDS. This isn't the case.”

This has been echoed by Peter Flegg (“Re: Re: Oxidation – the primary cause for AIDS and “HIV””, 25 January 2005): “The problem with the Perth Group's oxidative stress theory is that it is logically inconsistent. Nicholas Bennett has neatly exposed at least one major flaw within it, namely that those with oxidative stress but without HIV do not get AIDS (or at least do not develop severe immunodeficiency which results in opportunistic infections).”

Surely they are both aware that, for example, individuals who are treated with chemotherapy and the so-called “immunosuppressive therapy” which are oxidising agents in the absence of “HIV” develop AIDS.

 

We are disappointed that instead of directly answering questions posed in our rapid response “Oxidation – the primary cause for AIDS and “HIV”” (21 January 2005), Nicholas Bennett goes into a long speculative diatribe.   Would Nicholas Bennett please directly answer the following questions:

Is it true that the presently available evidence shows that:

(a) The tissues of AIDS patients and those at risk are oxidised (have decreased SH levels)?

Yes or no.

(b) The SH levels significantly predict survival?

Yes or no.

(c) There is a direct relationship between SH levels and T4 cell counts?

Yes or no.

(d) In vitro, the phenomena which are said to prove the existence of "HIV" cannot be detected unless the cultures are oxidised and can be inhibited by antioxidants?

Yes or no.

(e) In vivo, there is an inverse correlation between the SH levels and the "HIV" load?

Yes or no.

If the answers to question (a-e) are yes does it not mean then that the presently available evidence provides significant support for our non-retroviral theory of AIDS and "HIV"?

Yes or no

If any of the answers to question (a-e) is no, would Nicholas Bennett please give us references to the scientific evidence supporting his answer.   He should not debate if he doesn’t have any scientific evidence.   Opinions and/or “scientific thought” do not count.

 

 

References

(1) Papadopulos-Eleopulos E.  Reappraisal of AIDS – Is the Oxidation Induced by the Risk Factors the Primary Cause? Medical Hypothesis 1988; 25:151-162.

(2) Melbye M, Biggar RJ, Ebbesen P, Sarngadharan MG, Weiss SH, Gallo RC, et al. Seroepidemiology of HTLV-III antibody in Danish homosexual men: prevalence, transmission, and disease outcome. British Medical Journal (Clinical Research Edition) 1984;289:573-5.

(3) Stevens CE, Taylor PE, Zang EA, Morrison JM, Harley EJ, de Cordoba SR, et al. Human T-cell lymphotropic virus type III infection in a cohort of homosexual men in New York City. Journal of the American Medical Association 1986;255:2167-2172.

(4) Caceres CF, van Griensven GJP. Male homosexual transmission of HIV-1. AIDS 1994;8:1051-1061.

Competing interests: None declared