HAART makes things worse: Elsevier journal publishes HIV/AIDS heresies
Posted by Henry Bauer on 2010/11/03
Tony Lance alerted me to a discussion on Questioning AIDS started by trueverax with links to some fascinating recent articles about “HIV” and oxidative stress, for example, Gil et al., “Altered oxidative stress indexes related to disease progression marker in human immunodeficiency virus infected patients with antiretroviral therapy”, Biomedicine & Pharmacotherapy (2010), doi:10.1016/j.biopha.2010.09.009; the journal is published by Elsevier Masson France.
This in-press article in an Elsevier journal seems no less heretical than those Elsevier withdrew a year ago from Medical Hypotheses after protests from HIV/AIDS vigilantes. As Tony had remarked, “The opening line probably caused the Perth Group to chuckle — or sob”. Indeed:
“It is generally accepted that oxidative stress (OS) is implicated
in immunological and metabolic abnormalities during HIV infection”
Beginning in the 1980s, the Perth Group has argued:
“That AIDS and all the phenomena inferred as ‘HIV’ are induced by changes in cellular redox brought about by the oxidative nature of substances and exposures common to all the AIDS risk groups and to the cells used in the ‘culture’ and ‘isolation’ of ‘HIV’”.
“There is no compelling reason for preferring the viral hypothesis of AIDS to one based on the activity of oxidising agents” — Eleni Papadopulos-Eleopulos, “Reappraisal of AIDS: Is the oxidation induced by the risk factors the primary cause?”, Medical Hypotheses 25 (1988)151-162.
The remarkable statement in the Abstract of Gil et al’s article, that the presence of oxidative stress in “HIV/AIDS” is “generally accepted”, is repeated in the text in this way:
“The redox balance is also severely disturbed in HIV infected individuals without HAART [7–13].” Those references are:
 Israel et al., Cellular and Molecular Life Sciences, 53 (1997) 864-70.
 Romero-Avila et al., Medical Hypotheses, 51 (1998) 169-73.
 Sönnerborg et al., Scandinavian Journal of Infectious Diseases, 20 (1988) 287-90.
 Favier et al., Chemico-biological Interactions, 91 (1994) 165-80.
 Allard et al., American Journal of Clinical Nutrition, 67 (1998) 143-7.
 Gil et al., Pharmacological Research, 47 (2003) 217-24.
 Pasupathi et al., Journal of Scientific Research, 1 (2009) 370-80.
I noticed that these seven articles, as well as the one in Biomedicine & Pharmacotherapy, are all in journals that do not specialize in HIV/AIDS. Yet the substance of these articles concerns HIV/AIDS more directly than it does anything else. Here’s a little research project for someone who has some time: Ask the authors of these articles whether they had tried to publish in a journal like JAIDS; and if not, why not?
Here’s another interesting fact about these articles: All the work was done outside the United States. Gil et al. worked in Cuba; Israel et al. in France; Romero-Alvira in Spain; Sönnerborg et al. in Sweden; Favier et al. in France; Allard et al. in Canada; Gil et al., 2003, in Cuba but with a co-worker in Italy; Pasupathi et al. in India.
It may not seem surprising, therefore, that none of these articles acknowledge research support from an American source. That is, it may not seem surprising to people not familiar with the fact that the National Institutes of Health (as well as a number of American foundations) do support considerable amounts of research outside the United States. Perhaps especially about HIV/AIDS; much research on HIV/AIDS in Africa, for example, is supported by American money.
But then again, it’s certainly no surprise that the National Institutes of Health would not support research on the role of oxidative stress in the conditions that are labeled “HIV-positive” or “AIDS”.
The discussion on Questioning AIDS also cites another study, from Africa, that reports correlation of “HIV-positive” status with lowered antioxidant activity: Bilbis et al., Annals of African Medicine, 9(#4) (2010) 235-9; not an AIDS-specialist journal, no research support acknowledged.
Now Gil et al. do not state outright that oxidative stress might be the cause of “HIV-positive” or of “AIDS”, they only point out that oxidative stress is present in those conditions. However, given that “HIV” virions have never been isolated from “HIV-positive” individuals, it is no great step from these findings to the stance taken by the Perth Group for more than two decades.
None of these articles cite the Perth work, of course. Even Romero-Alvira, who published in Medical Hypotheses in 1998, does not cite the 1988 Papadopulos-Eleopulos article in Medical Hypotheses.
* * * * * * * *
But the greatest heresy of Gil et al. (2010) lies not in pointing out the role of oxidative stress in HIV/AIDS: It is the finding, in a placebo-controlled trial, that HAART makes things worse.
A variety of measures of oxidative stress were used. Three groups of “HIV-positive” individuals were studied: One not subjected to antiretroviral drugs; one treated with AZT/3TC/ IND (zidovudine or Retrovir, a NRTI; lamivudine, a NRTI; indinavir, a protease inhibitor); one treated with D4T/3TC/ NEV (stavudine, Zerit, a NRTI; lamivudine, a NRTI; nevirapine or Viramune, a NNRTI):
“both combination . . . produced an increase in OS [oxidative stress] indexes paralleled to HIV progression marker change”; in the second (D4T) group to the extent that there was “a poor prognostic” under this treatment.
References are cited for the toxicity of HAART, including typical damage to mitochondrial function. The mitochondria are the energy-producing sites of all animal cells and play a significant role in the redox systems within all cells.
Perhaps most significant, it is pointed out that the surrogate markers typically used to assess the success of HAART, CD4 counts and viral load, did show “improvement” under HAART in these studies at the same time as oxidative stress increased:
“increasing OS . . . occurs . . .
during apparently successful HAART.
This . . . underline[s] HAART associated toxicity”
This work serves to explain quite a few things about “HIV/AIDS” and HAART, for example that neither CD4 counts nor viral load is a good predictor of clinical outcomes (Rodriguez et al., JAMA, 296 (2006) 1498-1506).
Another reference cited in this thread on Questioning AIDS confirms the finding of increased oxidative stress as a result of HAART:
“HAART may affect oxidative stress in HIV-1-infected patients
. . . antiretroviral therapy plays an important role
in the synergy of HIV infection and oxidative stress”
(PMID: 19884983, Mandas et al., Journal of Biomedicine & Biotechnology, 2009;2009:749575. Epub 2009 Oct 26 — again, not an AIDS-specialist journal; work done in Italy).
This entry was posted on 2010/11/03 at 12:49 pm and is filed under antiretroviral drugs, clinical trials, experts, HIV as stress, HIV does not cause AIDS, HIV skepticism. Tagged: oxidative stress. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.