HIV/AIDS Skepticism

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

Posts Tagged ‘mitochondrial toxicity of antiretroviral drugs’

Hidden in plain sight: The damage done by antiretroviral drugs

Posted by Henry Bauer on 2011/07/25

What’s plain to those not indoctrinated
evades the consciousness of the HIV/AIDS gurus

“hid these things from the wise and prudent, and
. . . revealed them unto babes”
(Luke 10: 21)

One of the features of the HIV/AIDS phenomenon, seemingly astonishing and indeed incredible if one has trust in modern medical science, is that the mainstream literature is replete with documented, reproducible contradictions of standard shibboleths disseminated by mainstream sources.
Weiss & Cowan  point out that there’s no gold-standard HIV test, that there’s no such thing as a “confirmatory” test, that no HIV test can diagnose HIV infection, and that a large number of positive tests are false positives; yet mainstream practice continues to ignore these facts, and public defenders of the faith blather on about the desirability of universal testing.
Jay Levy  has enumerated all the things about HIV/AIDS that are not known — namely, all the central matters like how HIV could possibly do what it’s alleged to do.
And when antiretroviral drugs are mentioned, they are routinely described as life-saving — even though the literature is full of evidence that the drugs are anything but life-saving and instead are highly toxic. The Treatment Guidelines issued by the National Institutes of Health — and which need modification several times a year! — admitted long ago that the majority of “adverse events” experienced by PWAs on antiretroviral treatment are non-AIDS events, namely, organ failures and cancers linked directly to the antiretroviral drugs (see “Death, antiretroviral drugs, and cognitive dissonance”, 9 May 2008). The toxicity of AZT was demonstrated in the very earliest clinical trial, and plaudits to the life-saving benefits of antiretroviral treatment judiciously omitted to claim benefits for the AZT and monotherapy era; yet practice continues to ignore the deadly nature of AZT and its ilk and they continue to be prescribed in the HAART cocktails; albeit not as AZT but as Retrovir or zidovudine or other NRTIs with even more exotic and unfamiliar names.
A very general type of damage done by antiretroviral drugs is to the mitochondria, the energy-producing centers of all our cells. Mitochondria have their own DNA, and damage to them is a life-long burden; it’s irreversible. It’s been known for a long time that the antiretroviral treatment of pregnant “HIV-positive” women, purportedly to prevent transmission of HIV, actually damages the mitochondria of the babies; see for instance the studies cited in “What HIV drugs do” (2007/12/15); “First: Do no harm!” (2007/12/19); “Poison in South Africa” (2008/10/26); “Protease inhibitors cause oxidative stress” (2009/04/25); “Human cancers (≥20% of them) are caused by viruses!” (2010/01/23); “HAART makes things worse: Elsevier journal publishes HIV/AIDS heresies” (2010/11/03).
In my anything-but-exhaustive files I find mention of damage to the mitochondria in many places. The central point is that antiretroviral drugs commonly used in HAART induce “mitochondrial toxicity . . . linked to severe side effects including lipodystrophy, peripheral neuropathy, hepatic steatosis, myopathy, cardiomyopathy, pancreatitis, bone marrow suppression, and lactic acidosis” — Hendrickson et al., “Mitochondrial DNA haplogroups influence AIDS progression”, AIDS 22 (2008) 2429-39; citing
— Kohler & Lewis, “A brief overview of mechanisms of mitochondrial toxicity from NRTIs”, Environmental and Molecular Mutagenesis 48 (2007) 166-72
— Lewis, “Nucleoside reverse transcriptase inhibitors, mitochondrial DNA and AIDS therapy”, Antiviral Therapy 10 (Suppl 2, 2005) M13–27
— Lewis et al., “Antiretroviral nucleosides, deoxynucleotide carrier and mitochondrial DNA: evidence supporting the DNA pol gamma hypothesis”, AIDS 20 (2006) 675-84
—Brinkman et al., “Mitochondrial toxicity induced by nucleoside-analogue reverse-transcriptase inhibitors is a key factor in the pathogenesis of antiretroviral-therapy-related lipodystrophy”, Lancet 354 (1999) 1112-5
— Chapplain et al., “Mitochondrial abnormalities in HIV-infected lipo-atrophic patients treated with antiretroviral agents”, JAIDS 37 (2004) 1477-88
— Brinkman et al., “Adverse effects of reverse transcriptase inhibitors: mitochondrial toxicity as common pathway”, AIDS 12 (1998) 1735-44
Other references in my files to mitochondrial damage by antiretroviral drugs include articles from as far back as 1995, indicting in particular the NRTIs that continue to be part of many HAART regimens:
— Lewis & Dalakas, “Mitochondrial toxicity of antiviral drugs”, Nature Medicine 1 (1995) 417-22
Later articles (including those already cited) indict not only AZT and other NRTIs but other components of HAART as well:
— Donovan (editorial), “A new challenge for the neuroradiologist: MR recognition of mitochondrial dysfunction in children born of HIV-seropositive mothers on antiretroviral therapy”, American Journal of Neuroradiology 26 (2005) 687-9, which cites the following 13 sources from as far back as 1989:
— Blanche et al., “A prospective study of infants born to women seropositive for human immunodeficiency virus type I: HIV infection in newborns — French collaborative study group”, New England Journal of Medicine 320 (1989) 1643-8
— Connor et al., “Reduction of maternal-infant transmission of human immunodeficiency virus type I with zidovudine treatment”, New England Journal of Medicine 331 (1994) 1173-80
— Munoz et al., “Mitochondrial diseases in children: neuroradiological and clinical features in 17 patients”, Neuroradiology 41 (1999) 920-8
— Blanche et al., “Persistent mitochondrial dysfunction and perinatal exposure to antiretroviral nucleoside analogues”, Lancet 354 (1999) 1084-9
— Culnane et al., “Lack of long-term effects of in utero exposure to zidovudine among uninfected children born to HIV-infected women: Pediatric AIDS Clinical Trials Group Protocol 219/076 Teams”, JAMA 281 (1999) 151-7
— Gerschenson et al., “Fetal mitochondrial heart and skeletal muscle damage in erythrocebus patas monkeys exposed to in utero to 3′-azido-3′-deoxythymidine [AZT]”, AIDS Research & Human Retroviruses 16 (2000) 635-44
— Perinatal Safety Review Working Group, “Nucleoside exposure in the children of HIV-infected women receiving antiretroviral drugs: absence of clear evidence for mitochondrial disease in children who died before 5 years of age in five United States cohorts”, JAIDS 25 (2000) 261-8
— Taylor & Low-Beer , “Antiretroviral therapy in pregnancy: a focus on safety”, Drug Safety 24 (2001) 683-702
— Mantovani & Calamandrei, “Delayed developmental effects following prenatal exposure to drugs”, Current Pharmaceutical Design 7 (2001) 859-80
— Barret et al., “Mitochondrial dysfunction in HIV uninfected children”, AIDS 17 (2003) 1769-85
— Shiramizu et al., “Placenta and cord blood mitochondrial DNA toxicity in HIV-infected women receiving nucleoside reverse transcriptase inhibitors during pregnancy”, JAIDS 32 (2003) 370-4
— Poirier et al., “Long-term mitochondrial toxicity in HIV-uninfected infants born to HIV-infected mothers”, JAIDS 33 (2003) 175-83
— Tardieu et al., “Cerebral magnetic resonance imaging in children born to HIV seropositive mothers and perinatally exposed to zidovudine”, American Journal of Neuroradiology 26 (2005) 695-701.
And there are articles more recent than that survey as well, for example
— Saitoh et al., “Impact of Nucleoside Reverse Transcriptase Inhibitors on mitochondria in Human Immunodeficiency Virus Type 1-infected children receiving Highly Active Antiretroviral Therapy”, Antimicrobial Agents and Chemotherapy, 51 (2007) 4236-42
“New chemical tool kit manipulates mitochondria, reveals insights into drug toxicity”, ScienceDaily.

Connoisseurs of how to design clinical trials to get the desired results may notice among these many titles reporting damage the couple that seek to downplay it: Culnane et al. claiming — in 1999!! — “lack of long term effects” for AZT damage to fetuses; and the Perinatal Group’s “absence of clear evidence” in children who died before age 5 [my emphases]. The Culnane study reported only for a median age of 4.2, which is hardly “long term”, and 3 of 122 of those children had already shown “unexplained” adverse ophthalmic or cardiac effects. An important point about the irreversible damage to mitochondria is that it’s irreversible, affects all cells in the body, and is best described overall as premature aging, bringing greater probability of just about every type of non-infectious ailment. Lack of “clear” evidence of harm before age 5 is neither here nor there insofar as mitochondrial damage is concerned. These poor children have been irremediably harmed and robbed of any chance of a long and healthy life.

I’ve cited so many articles for several reasons; it’s easy to do because there’s such a plethora of them. The HIV/AIDS vigilantes’ typical defense, that we Rethinkers cherry-pick the literature, is utterly impossible here. Moreover, the deluge of studies finding the same thing illustrates some of the dysfunction of modern medical “science” and practice. The same things are “studied” over and over again, because the purpose is to “do research”, to earn livings through getting grants and doing research, with the production of useful knowledge to improve medical applications merely an occasional byproduct. Also illustrated is that highly reproducible results do not alter medical practice when those results contradict mainstream dogma.
For a long time, many years if not a couple of decades, it’s been known that antiretroviral treatment causes damage to mitochondria. Nevertheless, untold numbers of people, including pregnant women and babies, continue to be subjected to this iatrogenic harm.
Even in terms of mainstream dogma, this life-long damage is inflicted for absolutely no reason in many cases since the “HIV” tests have so great an incidence of undoubted false positives. (Undoubted even in mainstream terms and accepting mainstream views that HIV is real, see Weiss &Cowan, “Laboratory detection of human retroviral infection”, chapter 8 in Wormser, AIDS and Other Manifestations of HIV Infection, 2004).
It’s as though practice and “research” exist in parallel universes that rarely if ever communicate meaningfully with one another. Indeed, it seems that there’s not much meaningful communication even within the research community, since well known facts continue to be “discovered” and regarded as publishable. Thus Payne et al. appear to have discovered in 2011 that antiretroviral drugs damage the mitochondria: “Mitochondrial aging is accelerated by anti-retroviral therapy through the clonal expansion of mtDNA mutations”, Nature Genetics, published online 26 June 2011; doi:10.1038/ng.863. The 28 references given in this latest discovery of mitochondrial damage from antiretroviral drugs do not include any of those earlier discoveries of this effect that I’ve cited above.
What position does officialdom take? In particular, the Food and Drug Administration which is charged with approving drugs only if they are safe and effective? Does it act to withdraw drugs found to be toxic, to cause irreversible life-long damage that leads to premature aging and early organ failures?
Of course not:
“The problem of mitochondrial toxicity is now sufficiently well-recognized that the FDA recently released recommendations that all new antiviral drug candidates should be screened for toxicity to mitochondria” [emphasis added].
What’s needed, in other words, is more research. For example, to invent a test by which to screen potential drugs for mitochondrial toxicity:
MitoSciences announces  that it has just been awarded $590,000 by the National Institutes of Health to support the development of companion diagnostic tests for antiviral drugs. . . . Many of these drugs are known to cause toxic side effects, often due to inhibition of mitochondrial function. . . . MitoSciences has demonstrated that its tests can identify drug toxicity early, often before outward signs of the conditions can be observed clinically.”
In the meantime, drugs already known to damage mitochondria continue to be prescribed, and there are even continual calls to make more of them available to people and countries that cannot afford to pay for them.

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