Oxidation - the primary cause for AIDS and "HIV" 21 January 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: Oxidation - the primary cause for AIDS and "HIV"

Oxidation - the primary cause for AIDS and "HIV"

 

In his rapid response: "Reply to James Whitehead", 3rd January, Nicholas Bennett wrote:  "My personal take on the GSH issue is hinted at in the post Mr Whitehead made.  Pre-HAART HIV-infected patients appear to have lower levels of GSH and (interestingly enough) the stereotypical "antioxidant" vitamins.  It seems clear that HIV itself induces GSH reduction itself, either directly or through the chronic overstimulation of the cellular immune system (a hypercatabolic state)".

 

Firstly, AIDS patients have abnormal GSH levels both before and post HAART treatment.  Even if the GSH levels return to normal after HAART it does not mean the cause of the decrease is HIV.  In his rapid response: "Re: Re: Reply to James Whitehead", 8th January and "Re: Re: HIV-1 does not encode glutathione peroxidase", 14th January, Nicholas Bennett gave a long (irrelevant and sometimes confusing and contradictory) yarn but no evidence which shows HIV is the cause of the oxidation in AIDS patients.

 

Let us remind Nicholas Bennett of a few facts:

 

In our paper "Oxidative stress, HIV and AIDS", published in 1992 in Research and Immunology, an Institut Pasteur publication, we wrote:   "At first sight it appears that there is no common factor, apart from HIV infection, linking the various AIDS risk groups.  However, homosexuals are exposed to relatively high levels of nitrites and anally deposited sperm, drug abusers to opiates and nitrites, haemophiliacs to factor VIII.  All these are known potent oxidising agents which oxidise many cellular reducing equivalents such as NADPH and all sulphydryl groups, including those of cysteine (acid-soluble thiols) (Papadopulos-Eleopulos, 1988)”.1

 

Would Nicholas Bennett please tell us:

 

(a)        Does he agree with us that semen, nitrites, opiates, factor VIII are oxidising agents and that one of the consequences of malnutrition is oxidation?

                                                Yes or no

 

(b)        If yes, then given the fact that our evidence that the AIDS patients and those at risk are exposed to strong oxidising agents has been in the scientific literature for nearly 17 years, what is the reason that the "HIV" experts ignore these agents and claim that the cause of oxidation is:

 

(i)         "HIV";

(ii)        "several mechanisms - such as low intake of antioxidants or their precursors, malabsorption, and, in peripheral tissue, enhanced cysteine metabolism with a consequent loss of sulfur";2

(iii)       "Multiple mechanisms may contribute to systemic GSH deficiency in HIV disease, including excessive production of inflammatory cytokines and excessive use of GSH-depleting drugs";3 and the only advice given to the patients is:  “At a more immediate level, the demonstration here that prognosis worsens as GSH levels decrease suggest that certain precautions be taken to minimise GSH deficiency in HIV-infected individuals.  In general, it may be prudent for these individuals to avoid excessive exposure to UV irradiation and unnecessary use of drugs that can deplete GSH - e.g. alcohol and prescription or over-the-counter formulations containing acetaminophen”.3

 

Would Nicholas Bennett please tell us:

 

(a)        Is it true that a theory is as good as its predictions?

                                                Yes or no.

 

(b)        If yes:

 

(i)         what are the main predictions of the "HIV" theory of AIDS?

(ii)        what is the presently available evidence which supports them?

 

In our "Oxidative stress, HIV and AIDS" 1992 paper we wrote:  "As long ago as 1983, one of us (E.P.-E.) proposed that oxidative mechanisms are of critical significance in the genesis of AIDS (acquired immune deficiency syndrome).  A prediction of this hypothesis was that the mechanisms responsible for AIDS could be reversed by the administration of reducing agents, especially those containing sulphydryl groups (SH groups).  The discovery of HIV resulted in a broadening of this hypothesis in that it considered oxidative stress as a principal mechanism in both the development of AIDS and expression of HIV (Papadopulos-Eleopulos, 1988;  Papadopulos-Eleopulos et al, 1989)". 

 

That is the main predictions of our oxidative theory of AIDS were:

 

(a)        In AIDS patients and those at risk there would be a decrease in the reducing equivalents in general and of the SH groups in particular;

 

(b)        AIDS may be prevented and treated by:

 

(i)         ceasing exposure to the oxidising agents to which patients belonging to the AIDS risk groups are subjected;

(ii)        correcting malnutrition;

(iii)       administration of antioxidants and in particular sulphydryl (SH) components.1 4-7

 

(c)        The phenomena which are claimed to prove the existence of "HIV" are the result of oxidation and thus can be prevented and inhibited by antioxidants, in particular SH compounds.

 

Would Nicholas Bennett please tell us:  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.

 

 

REFERENCES

 

1. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Oxidative stress, HIV and AIDS. Res Immunol 1992;143:145-8. http://www.theperthgroup.com/SCIPAPERS/oxstresshivaids.html

2. Aukrust P, Muller F, Svardal AM, Ueland T, Berge RK, Froland SS. Disturbed glutathione metabolism and decreased antioxidant levels in human immunodeficiency virus-infected patients during highly active antiretroviral therapy--potential immunomodulatory effects of antioxidants. J Infect Dis 2003;188:232-8.

3. Herzenberg LA, De Rosa SC, Dubs JG, Roederer M, Anderson MT, Ela SW, et al. Glutathione deficiency is associated with impaired survival in HIV disease. Proc Natl Acad Sci U S A 1997;94:1967-72.

4. Papadopulos-Eleopulos E. Reappraisal of AIDS: Is the oxidation caused by the risk factors the primary cause? Med Hypotheses 1988;25:151-162. http://www.theperthgroup.com/SCIPAPERS/reappraisalofaids.html

5. Papadopulos-Eleopulos E. Looking back on the oxidative stress theory of  AIDS. Continuum 1998;5:30-35. http://www.theperthgroup.com/CONTINUUM/lookingback.html

6. Papadopulos-Eleopulos E, Hedland-Thomas B, Causer DA, Dufty AP. An alternative explanation for the radiosensitization of AIDS patients. Internat J Radiat Oncol Biol Phys 1989;17:695-697.

7. Turner VF. Reducing agents and AIDS--Why are we waiting? Med J Aust 1990;153:502.

 

Competing interests: None declared