Elsevier publishes another HIV-denialist article
Posted by Henry Bauer on 2010/01/13
“[T]here is extensive evidence that certain micronutrient deficiencies are associated with faster disease progression or increased mortality risk, and that dietary supplements . . . can prolong survival in HIV/AIDS. . . .
one aspect stands out in importance: the potential relationship to oxidative stress. . . . the antioxidant role of selenium in glutathione peroxidases . . . .
a daily supplement of 200 μg of selenium alone stopped progression of HIV-1 viral load increases, and lead [sic] to improved CD4 counts. . . . selenium status was reported to be 10 times more significant than CD4 cell count as a predictor of mortality. . . .
HIV infection is typically characterized by a dramatic decline in glutathione levels . . . [which] suggests an abnormal degree of biological oxidation, manifesting as elimination of cysteine sulfur as sulfate. A key feature of HIV disease is an apparent ‘antioxidant defect’ . . . [which] can be aggravated by co-factors such as malnutrition, co-infection with other microorganisms, and the use of various oxidant drugs, such as nitrites. . . .
Intermediates of oxidative tryptophan metabolism have also been implicated in neurotoxicity, potentially contributing to AIDS dementia. . . .
oxidative stress can induce niacin/NAD+ depletion. . . .
The oxidative stress-induced niacin sink (OSINS) model for HIV pathogenesis. . . . links oxidative stress and selenium to the observed tryptophan abnormalities and immunosuppression in HIV/AIDS. . . . [and] provides a mechanism whereby oxidative stress associated with HIV infection can contribute to immunosuppression via tryptophan deletion, as well as neurotoxicity via toxic tryptophan metabolites and ATP depletion. . . .
But whatever the source of oxidative stress, there would be a net effect towards niacin depletion and compensatory tryptophan oxidation. . . .
the need for certain nutrients in HIV infection may be largely secondary to an underlying defect that could be largely rectified by another nutrient, with antioxidants being the most fundamental to an effective regimen. . . .
whatever underlies or contributes to the antioxidant defect and increased oxidative stress . . . leads also to intracellular niacin depletion, and thereby to tryptophan depletion, with an end result of immunosuppression . . . and also T-cell loss” [emphases added].
It might seem natural to infer that this was written by the Perth Group, who have argued for upwards of two decades that “AIDS” results from oxidative stress, possibly with co-authorship by Rebecca Culshaw, who described the crucial role of glutathione, and by Harold Foster, who has long argued the central role of selenium, not to mention Matthias Rath, who has long spoken up for the value of micronutrients in treating AIDS patients.
But no. What’s more, none of those earlier publications are mentioned in this article by Ethan Will Taylor, “The oxidative stress-induced niacin sink (OSINS) model for HIV pathogenesis”, published on-line in Toxicology (Received 1 July 2009 — Received in revised form 10 October 2009 — Accepted 15 October 2009 — On-line at PubMed 24 October [Epub ahead of print, PMID: 19857540, ).
(The review is described as “Hypothesis”, suggesting it might equally have been accepted by another Elsevier journal, Medical Hypotheses, were it not that the latter seems nowadays to bar anything that questions HIV/AIDS orthodoxy.)
At any rate, this article talks about “HIV-associated” oxidative stress and the benefits of nutritional supplements in “HIV-infected” people without demonstrating that “HIV” is actually involved. Essentially the same network of reactions and feedback applies in any situation of oxidative stress, as noted in the article: “whatever the source of oxidative stress . . . whatever underlies or contributes to the antioxidant defect and increased oxidative stress”. The only suggested involvement of HIV in the network of reactions is via a postulated stimulation of IDO (indoleamine-2,3-dioxygenase) by tat and nef proteins and an increased level of interferon γ ascribed to viral infection and immune activation.
If it could be shown that under generalized oxidative stress, substances are released that are capable of yielding an “HIV-positive” response, that would combine with this comprehensive review of the literature to make oxidative stress an entirely plausible cause of AIDS, a worthy alternative to the HIV/AIDS hypothesis.
In point of fact, it is already well and long known that “HIV-positive” is a condition that can be brought on by a large range of conditions and infections: hypergammaglobulinemia, tuberculosis, or vaccination against flu, and dozens more documented by Christine Johnson (“Whose antibodies are they anyway? Factors known to cause false positive HIV antibody test results”, Continuum, #3, Sept./Oct. 1996, p.4, anti-tetanus shots (Saag et al., Nature Med 1996;2:625-9 and Gonnelli et al., Lancet 1991;337:731), and even pregnancy (Taha et al., AIDS 1998;12:197-203; Gray et al., Am J Obstet Gynecol 2001;185:1209-17; Gray et al., Lancet 2005;366:1182-8). Drug abusers very often test “HIV-positive”. That the Centers for Disease Control and Prevention included increasing numbers of conditions as “AIDS-defining” after “HIV-positive” became a criterion reflects the fact that many illnesses induce oxidative stress and the resulting “HIV-positive” status.
Here is a simple way of Rethinking AIDS:
There are two hypotheses.
1. AIDS is caused by a previously unknown retrovirus that first infected gay men simultaneously in several large metropolitan areas in the United States even though it had first crossed into humans in Africa. No vaccine or microbicide against it has been found after more than two decades of concentrated effort. Transmitted sexually, it is however very difficult to transmit, which is why it has remained within the original risk groups of promiscuous drug-abusing gay men and other drug abusers, except in Africa where 20-40% of the adult population has several sexual partners simultaneously and changes them frequently (James Chin, The AIDS Pandemic); however, the retrovirus has never actually been observed, in prospective studies, to be transmitted sexually. It kills T-cells by some unknown but certainly indirect as well as obscure mechanism. Though transmitted by breastfeeding, it is transmitted less, the greater the degree of exclusive breastfeeding. The presence of antibodies denotes active infection even when no actual virus can be detected. Some significant proportion of those infected remain healthy, even as no reason for this immunity has been discovered. One of the three original salient AIDS diseases supposedly caused by this retrovirus, Kaposi’s sarcoma, turns out not to be caused by it after all. Antibodies to the retrovirus appear after vaccination against flu, or after an anti-tetanus shot, and in a host of illnesses as well as natural conditions of some physiological stress like pregnancy. In an appreciable number of AIDS cases, no antibodies or retrovirus could be found, but this could be explained away as another new disease, idiopathic CD4-T-cell lymphopenia. Drugs that kill the virus do not correlate with restoration of the immune system nor with improved health. Indeed, purported restoration of the immune system with these drugs brings on another new ailment, “immune restoration syndrome”, a worsening of clinical condition with symptoms that mimic AIDS. The retrovirus mutates at unprecedented speed, so that infected individuals harbor not a single variant but a swarm of variants; and all variants and strains appear to be pathogenic to similar extents. Antiretroviral treatment is by toxic drugs whose side effects are so severe that non-compliance by patients has been observed or estimated at nearly 50%. Deaths from AIDS continue to occur in the same age-range as before, roughly mid-30s to late 40s. Although the retrovirus is latent for an average of a decade before causing illness, the age of first infection, of first AIDS diagnosis, and of death are all in that same age range.
2. AIDS is caused by oxidative stress. Proof: dietary supplements of antioxidants and essential minerals and vitamins restore health and extend life without dangerous side effects.