Stumbled upon this while looking for something else...
Asking the scientists in the group - is there any merit?
Is it possible according to this theory that AIDS could be treated prophylactically by NAC, Vascepa, or 2-73?
The first and only study which supports the prediction of our theory – that AIDS can be prevented and treated by stopping exposure to the oxidising risk factors and by using “currently available therapeutic [antioxidants in general and SH-containing, in particular] substances” was conducted by Leonore and Leonard Herzenberg and their colleagues from Stanford University. First they sought data to show a relationship between SH concentration (reduced glutathione, GSH) and survival in AIDS patients. They showed “that GSH levels are lower in subjects with CD4 T cell counts below 200/µl (CD4<200) than in subjects at earlier stages of HIV disease: that among subjects with CD4<200, lower levels of GSB [glutathione-S-bimane fluorescence = a measure of the intracellular GSH concentration] predict decreased survival; and that the probability of surviving 2-3 years increases dramatically as GSB levels approach normal range”.36
Second they conducted a randomised, double-blind placebo-controlled trial to determine if the GSH can be replenished by oral administration of N-acetylcysteine (NAC) for 8 weeks. They showed that NAC increased whole blood GSH levels and the effect was more effective in the subjects who had the lowest levels at the start of the trial. After 8 weeks all patients were offered open-label NAC for up to 8 months. Although the study was not specifically designed to discover the effect of NAC on survival they reported “To our surprise, given the relatively short time (8-32 weeks) that NAC was administered, we found that NAC ingestion was associated with substantially longer survival…The association of prolonged survival in the oral administration of NAC in this study is very dramatic…[our study] established GSH as a key determinant of survival in HIV disease”.37
According to these researchers their study “established GSH deficiency as a key determinant of survival in HIV disease”. They further commented “Therefore, our findings basically argue for the initiation of a placebo-controlled trial designed specifically to determine the therapeutic value of NAC in AIDS and/or that of other GSH-replenishing drugs. Since NAC is nontoxic and could be used where medical services are limited, our findings indicate that such a trial should be initiated as soon as possible. Other pharmaceuticals that replenish GSH should also be tried for the same purpose. In any event, the poor survival that we have demonstrated in GSH-depleted subjects with AIDS underscores the importance of finding ways to replenish GSH in these individual and ways to prevent GSH depletion in the disease…However, HIV-infected individuals would be better served if we could identify the mechanisms that underlie the GSH depletion and intervene, if possible, to prevent its occurrence. If ways could be found to do this on a long-term basis, HIV disease progression might be controlled in a way that would prevent the worst aspects of the disease…At a more immediate level certain rather simple precautions might help to slow the progress of HIV disease. Since studies presented here associate GSH depletion oxidative stress with poor survival in AIDS, we believe that HIV-infected individuals should avoid excessive exposure to sun and UV irradiations and excessive use of drugs such as acetaminophen (Tylenol) [paracetamol] that are known to deplete GSH. Physicians treating HIV-infected individuals should similarly consider exercising caution in prescribing formulations or recommending over-the-counter preparations containing such GSH-depleting drugs. These conservative measures could eliminate some of the more accessible causes of GSH depletion and thus could potentially prevent decrease of GSH to the level that predicts death within the following 2 years”.37
Although there are numerous publications on “oxidative stress” and HIV and AIDS, and billions of dollars spent to deploy a large number and variety of drugs to treat HIV/AIDS patients (over 30 are approved at present), no HIV expert has thought it worthwhile to initiate a trial “as rapidly as possible” of the readily available, relatively non-toxic and inexpensive substances such as NAC or other SH containing compounds which the Herzenbergs urged in 1989 and we advocated at the beginning of the AIDS era.
At the time of writing a Medline search using the keywords [HIV and redox] resulted in 654 publications. Our hypothesis, Reappraisal of AIDS--is the oxidation induced by the risk factors the primary cause? 25th March 1988 is listed 654, that is, the first such publication on record at the National Library of Medicine. Although we were the first to propose a noninfectious redox theory of AIDS and identified the cause and “the mechanism that underlie[s] the GSH depletion” and thus to point the way “to prevent its occurrence” and its treatment, for reasons upon which we can only speculate, with one exception,38 no one refers to our numerous publications on this subject. This applies even to Dröge and the Herzenbergs although both were made aware of our work. It is also astonishing to read the scope of the Herzenbergs’ preventative measures: avoid UV exposure and paracetamol, as if these constituted the lion’s share of GSH depleting agents to which the AIDS risk groups are exposed.
Addendum: The oxidative theory, the Perth Group and Luc Montagnier In July 1991 a full-page advertisement appeared in Nature in which Pasteur Mérieux Sérums & Vaccins offered a Post-Doctoral Fellowship “designed to encourage the research on examining relationships between oxidative stress and HIV infection".39 We expected any scientist interested in this subject, including Montagnier, to be aware of our contribution to this topic.14 Nonetheless, following the advertisement we decided to make him personally aware of our theory,40 sending copies of the 1988 paper and two others, one of which was a recently completed draft on the pathogenesis of Kaposi’s sarcoma (later published in Medical Hypotheses19) Montagnier acknowledged receipt of our material in a letter dated 25th October 199141 stating “I will certainly return to you after reading them” but failed to do so.
After all this, in his book Virus42 Montagnier wrote: “Aside from a small number of pioneers – Dröge in Germany and Leonard and Lena Herzenberg in the United States – very few researchers have shown interest in this phenomenon [“oxidative stress”], despite its fundamental role in the illness…The phenomenon is massive, and occurs at an early stage”. As to its cause, “In addition to the virus, [HIV], all opportunistic agents can likewise contribute to oxidative stress, and from the very onset of infection, so can mycoplasmas”. Not only did Montagnier forget or ignore our group and our explicit evidence that cellular oxidation plays a “fundamental role in illness”, but, like the Herzenbergs, he forgot or ignored our list of oxidising agents to which the AIDS-risk patients are exposed. And that such exposures occur long before the patients develop HIV and opportunistic infections. Montagnier also seems unaware that it is oxidation which leads to the opportunistic infections. After all, it is his compatriot Pasteur who taught us “Bernard was right; the pathogen is nothing; the terrain is everything”.
Montagnier seems to have also forgotten that as far back as January 1986 he wrote “replication and cytopathic effect of LAV [HIV] can only be observed in activated T4 cells. Indeed, LAV infection of resting T4 cells does not lead to viral replication or to expression of viral antigen on the cell surface [that is, infection], while stimulation by lectins [mitogens] or antigens of the same cells results in the production of viral particles, antigenic expression and the cytopathic effect”.43 And that in our 1992 “Oxidative Stress, HIV and AIDS” paper18 which he must have also read, we presented evidence that cellular activation is an oxidative process and that oxidation is a prerequisite to detect the phenomena claimed to prove HIV infection. In other words, no activation, namely no oxidation = no infection.
We have also directly challenged Montagnier to defend “HIV” and the HIV theory and refute our theory in two scientific publications in 200444 and 2006.45 Although this matter was now in the public domain again Montagnier did not respond. Remarkably nowadays Montagnier accepts that in Africa the cause of AIDS is oxidation and advocates treating AIDS patients with antioxidants.46, 47 If Montagnier accepts oxidation as the cause of AIDS in Africa then why not in the other risk groups where individuals are exposed to strong oxidants?14 Nonetheless, since he accepts that in Africans (a) AIDS is due to oxidation; (b) oxidation is due to malnutrition (poverty48); it follows that the cause of AIDS in the vast majority of people is not HIV. This being the case, why not in the remaining minority?
The failure of an antibody to bind to a T4 cell does not prove the cell is missing or dead. In fact in 1985 Montagnier himself acknowledged that antibody binding to T cells is sensitive to their physiological state – “this phenomenon [antibody binding to T4 lymphocytes] could not be related to the cytopathic effect” of HIV but is “probably due to either modulation [modification, alteration] of T4 molecules at the cell membrane or steric hindrance of antibody-binding sites” 32 (steric hindrance “occurs when the large size of groups within a molecule prevents chemical reactions that are observed in related molecules with smaller groups” [Wikipedia]). That is, the T4 cells are present but the counting machine is blind to those to which the antibody cannot bind. Failure to bind is not limited to modulation or steric hindrance. T4 cells can change their phenotype from one subset to another, for example, to a T8 or T10 lymphocyte.26 As far back as 1982 it was shown that T4 cells become T8 cells following a 24 hour incubation with chemicals such as impromidine and adenosine.33 (Adenosine is a physiological substance as well as a drug frequently used in emergency medicine to treat cardiac arrhythmias). From the beginning it was known that in AIDS patients a decrease in T4 lymphocytes is accompanied by an increase in T8 lymphocytes with their total number remaining constant, that is, normal.34, 35 This means that T-cell markers are fluid, modulated by factors in their environment which include the physiological milieu of AIDS patients and those at risk of developing AIDS.36-39
