HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS

Posts Tagged ‘nelfinavir’

Protease inhibitors cause oxidative stress

Posted by Henry Bauer on 2009/04/25

Mainstream propaganda harps continually on the life-saving virtues of HAART, treatment that often combines a couple of reverse-transcriptase inhibitors and a protease inhibitor (PI). Indeed, it was the introduction of PIs that marked the beginning of David Ho’s “hit hard, hit early” approach that has become known as Highly Active AntiRetroviral Treatment.

Rethinkers and Skeptics who point to the  seriously debilitating “side” effects of HAART are brushed aside, even as the NIH’s Treatment Guidelines acknowledge that the majority of adverse events experienced by HAART-treated “AIDS” patients are owing to HAART and not to “AIDS”:
“In the era of combination antiretroviral therapy, . . . the risk of several non-AIDS-defining conditions, including cardiovascular diseases, liver-related events, renal disease, and certain non-AIDS malignancies . . .  is greater than the risk for AIDS in persons with CD4 T-cell counts >200 cells/mm3; the risk for these events increases progressively as the CD4 T-cell count decreases from 350 to 200 cells/mm3” (p. 13, January 2008 version).

The research literature, too, reveals what publicly disseminated propaganda refuses to acknowledge, for example, that PIs interfere drastically with fat metabolism and mitochondrial function, which includes absolutely-essential-to-life energy processes:

Public release date: 25-Mar-2009
Contact: Dr. Krishna C. Agrawal
Society for Experimental Biology and Medicine
. . . HIV-1 protease inhibitors (PIs), such as nelfinavir included in highly active antiretroviral therapy (HAART) regimen for the treatment of HIV-1 patients, induce deleterious effects on insulin secretion mediated through the oxidative stress pathway. . . . A significant decrease in ATP production was also observed . . . . This study appears in the April 2009 issue of Experimental Biology and Medicine. Although insulin resistance has been clinically observed in HIV-1 patients receiving HAART regimen, the molecular mechanisms of this metabolic abnormality have not been delineated.
. . . . Since the hypoglycemic effects of Nigella sativa oil have been investigated in the past, the investigators postulated that nelfinavir induced oxidative stress may be ameliorated by the administration of the active ingredient of this oil, thymoquinone. Furthermore, it was envisioned that since thymoquinone shares a structural homology with ubiquinone [commonly known as Coenzyme Q10] (mitochondrial component) it is likely that it may act as a mitochondrial antioxidant. . . . these findings clearly suggest a potential role for the use of black seed oil or thymoquione [sic] as a protective agent against HIV-1 protease inhibitor induced deleterious effects on pancreatic beta-cells”.

Reports like these are no doubt acceptable because they don’t stress the deleterious “side” effects of HAART but rather emphasize the “positive” approach of guarding against those “side” effects. Nevertheless, this is a back-door acknowledgement of how serious those “side” effects are.

Note too that when a traditional remedy is touted by mainstream researchers — here “Nigella sativa oil” or “black seed oil” — this is scientifically acceptable, whereas suggesting the benefits of traditional remedies is laughed out of court if proposed by the South African Minister of Health or by Dr. Matthias Rath (UCLA’s AIDS (“Beetroot”) Institute discovers how HIV kills cells, 2 January 2009; Mainstream pseudo-science good, alternative pseudo-science bad, 25 February 2009).

“Oxidative stress”, too, becomes scientifically acceptable when discussed in this context, but not when the Perth Group points to its explanatory power in relation to AIDS; nor does it bear mentioning that the oft-maligned Matthias Rath worked with Linus Pauling, who is arguably responsible for the wide recognition of the value of nutritional antioxidants like vitamin C.

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