FIRST: DO NO HARM!
Posted by Henry Bauer on 2007/12/19
That’s supposed to be the medical profession’s motto. If unsure whether available treatments will help, and especially if there’s a chance that they might harm—do nothing; practice “watchful waiting”.
HIV/AIDS practices take the opposite approach. In the determination to get rid of HIV, it is sometimes forgotten that the whole point is to make people better (WHAT HIV DRUGS DO, 15 December 2007).
“HIV-infection” has never been demonstrated in more than 1% of the immune-system cells that HIV supposedly targets. Antiretroviral drugs cannot discriminate between infected and non-infected cells of this class. To prevent the infected cells from producing more virus, we administer substances that kill all the cells. To get rid of 1 guilty party, we execute 100 or more innocent ones.
Cells are not persons, of course. But if we kill or damage enough innocent cells in a person—cells that are innocent but essential to health—, then we certainly harm and may kill that person.
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“Inasmuch as ye have done it unto . . . the least of these . . . , ye have done it unto me”
Babies are certainly persons.
It’s estimated that 15-30% of HIV-positive mothers pass “HIV infection” on to their babies—between 1 in 3 and 1 in 6 of their newborns are HIV-positive, in other words. To avoid that, HIV/AIDS experts recommend that all HIV-positive mothers be treated with substances that are known to produce serious damage to the babies. To perhaps safeguard 1 baby from the possible but not certain deleterious effects of HIV, harm is knowingly done to between 2 and 5 babies who would otherwise be healthy.
Dissidents would point out that this ratio, between 2 and 5 to 1, is excessively conservative. Being born HIV-positive does not prove the presence of active infection. Upwards of 75% of HIV-positive newborns revert spontaneously to HIV-negative in about the first year, because their HIV-positive test was triggered by “passive” antibodies transferred from the mother (see p. 97 ff. in The Origins, Persistence and Failings of HIV/AIDS Theory). So the odds are increased by a factor of at least 4: to prevent the birth of 1 “HIV-infected” baby, between 8 and 20 newborns who would otherwise be healthy are knowingly exposed to harm.
I said “possible but not certain” deleterious effects of “HIV infection” because
1. Some unknown proportion of HIV-positive people are “elite controllers” or “long-term non-progressors” who remain, untreated, in good health.
2. On average, it is supposed to take 10 years before “HIV infection” leads to symptoms of illness.
Research continues apace to develop better and less toxic treatments for “HIV infection”. Research continues apace for vaccines which, even if not effective in preventing “infection”, might nevertheless enable HIV-positive people to become, in effect, long-term non-progressors. With any luck, some success along those lines might be attained within a decade or so. That would be in time to help an appreciable proportion of babies now being born “HIV-infected”.
So: It is anything but certain that any given HIV-positive newborn will actually experience harmful consequences; and it is anything but certain, how serious those consequences will be if they do eventuate.
By contrast, the damage done by perinatal antiretroviral treatment is certain and serious. Very serious. Perinatal antiretroviral treatment brings both short-term and long-term harm, documented in considerable detail in the dozen-and-a-half articles in Environmental and Molecular Mutagenesis, 48, #3-4, April-May 2007, which a correspondent drew to my attention recently.
The lead review article (by Kohler & Lewis, pp. 166-72) cites “therapeutic experience”—that is, observations on human babies—that NRTIs, the backbones of standard antiretroviral treatment, damage the mitochondria.
Further: “Clinical and biological observations of mitochondrial dysfunction in children exposed to zidovudine (azidothymidine, AZT) during the perinatal period rapidly followed similar observations in animal experiments”—these were uninfected children born to HIV-infected mothers. One third of the babies had hyperlactatemia, which seemed to reverse within some months after treatment ceased but did sometimes lead to lactic acidosis, which can be life-threatening. Between 1 in 20 and 1 in 35 babies also developed severe neurological symptoms during the first 2 years of life, a phenomenon confirmed in several other studies (Benhammou et al., pp. 73-8).
Again, in the article by Sherine Chan et al. (pp. 190-200): “mitochondrial DNA (mtDNA) damage has been observed in both human and mouse neonates following perinatal exposure to AZT and AZT/3TC” as well as “NRTI-induced heart damage . . . in human infants”. Divi et al. confirm that “Transplacentally exposed human and monkey newborn infants show similar evidence of nucleoside reverse transcriptase inhibitor-induced mitochondrial toxicity”. Witt et al. (pp. 322-9) reiterate that “transplacental ZDV exposure is genotoxic in humans”.
One can predict with reasonable certainty that damage to the mitochondria of infants will have seriously debilitating consequences, probably during the whole span of a life that is also significantly shortened. Mitochondria are the energy centers of all mammalian cells. Their dysfunction can lead to a number of degenerative diseases and their deterioration over time, as mutations in their mtDNA accumulate, is one of the causes of senescence, perhaps even the most important one (Linnane et al., “Mitochondrial mutations as an important contributor to ageing and degenerative diseases”, Lancet 1989: 642-5 and further references in Linnane & Eastwood, Mitochondrion 2004: 1-11).
Should the children with damaged mitochondria live long enough, they are likely to contract cancers: “perinatal exposure to nucleoside analogs puts children at elevated risk of developing cancers later in life” (Wogan, pp. 210-4). In cultured cells, AZT produced “micronuclei, chromosomal aberrations, sister chromatid exchange, shortened telomeres, and other genotoxic effects” (Olivero, pp. 215-23). In experiments with mice, “Mutagenicity experiments with ABC [abacavir] alone, or in combination with AZT-3TC, were complicated by the extreme cytotoxicity of ABC” (Torres et al., pp. 224-38); “all NRTIs with antiviral activity against HIV-1 may cause host cell DNA damage and mutations, and impose a cancer risk” (Carter et al., pp. 239-47). “AZT, 3TC, and the combination of AZT and 3TC are transplacental mutagens” (Von Tungeln et al., pp. 258-69). Rats and mice dosed with AZT developed hemangiosarcoma (a “rare, rapidly growing, highly invasive variety of cancer”), mononuclear cell leukemia, liver cancers, and gliomas (brain tumors) (Walker et al., pp. 283-98); also “alveolar/bronchiolar adenomas and carcinomas . . . benign and malignant lung neoplasms”, since “incorporation of AZT or its metabolites into DNA, oxidative stress, and genomic instability may be the contributing factors to the mutation profile and development of lung cancer” (Hue-Hua Hong et al., pp. 299-306).
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AZT and its cousin NRTIs damage the mitochondria, whose proper functioning in all cells is essential to health. AZT and its cousin NRTIs also cause mutations that lead to all sorts of cancers.
The toxicity of AZT was known long before its introduction as an antiretroviral drug: it had been found too toxic to be used in cancer chemotherapy. Several of the papers cited above refer to similar damage in humans as in rats, mice, and monkeys: either there had not been studies in animals before the drugs were used in human beings, or the drugs were used in humans even though animal studies had shown cell and mitochondrial toxicities and carcinogenicity. Olivero (215-23) attempts an excuse: “Detailed information on the mechanisms underlying NRTI-associated antiretroviral efficacy, toxicity, and metabolic resistance were not available when AZT was first approved for use as an antiretroviral agent”; sure, “detailed information” wasn’t available, but it was certainly well known that AZT is toxic—see the oft-reproduced label below, and note the irony of “For laboratory use only. Not for drug, household, or other uses.” That’s how this chemical was described when it was introduced as an antiretroviral drug.
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Trying to understand how anyone could treat pregnant women and babies in this fashion, I can only conclude that the single-minded determination to wipe out HIV has outweighed all other considerations. Half-a-dozen of the cited articles emphasize that perinatal antiretroviral treatment has been shown to reduce mother-to-child transmission of HIV, as though this were the prime necessity by comparison to the damage known to be done by the drugs:
Acknowledged was “the necessity for effective protective strategies against NRTI-induced side effects” (Walker et al., 283-998). But what “protective” strategies are conceivable? Other than not using NRTIs, of course.
There is a repeated disingenuous call for careful monitoring of the damaged children, as though any amount of monitoring could undo the damage:
“the importance of continued surveillance of these children for increased cancer risk and . . . less genotoxic alternative agents” (Wogan, 210-4) ; “the mutagenic effects found in mother-child pairs receiving AZT-based treatments justify their surveillance for long-term genotoxic consequences” (Escobar et al., 330-43). “While these data support the continued use of AZT-based therapies during pregnancy, infants receiving prepartum AZT should be monitored long-term for adverse health effects” (Meng et al., 307-21). “Long-term monitoring of HIV-uninfected ZDV-exposed infants is recommended to ensure their continued health” (Witt et al., 322-9)–as though monitoring could “ensure continued health”!
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When AIDS was first noticed, the belief became embedded that it is inevitably fatal. When HIV was subsequently designated the cause of AIDS, the belief became that “HIV-positive” is inevitably fatal. That belief has continued to co-exist in company with its own disproof: the knowledge that some proportion of HIV-positive people (“elite controllers”, “long-term non-progressors”) never become ill, that HIV-positive people live a healthy life on average for 10 years before HIV-induced symptoms appear, and the shibboleth that “HIV is now a manageable disease”.
Damaging the mitochondria of newborns and subjecting them to significant risk of cancers is incompatible with current knowledge. A doubtful benefit to one newborn is being achieved at the cost of serious damage to at least 2, and perhaps 20 or more newborns who were never at any risk in the first place.
Is anyone reminded of burning witches at the stake in order to save their souls and wipe out the devils that had possessed them? Or, in more recent times, destroying a village in Vietnam in order to save it for democracy?
This entry was posted on 2007/12/19 at 2:49 pm and is filed under antiretroviral drugs, experts, HIV in children, HIV tests, HIV transmission, HIV varies with age, HIV/AIDS numbers. Tagged: antiretroviral drugs, antiretroviral treatment of babies, cancer side effects, drug toxicity, mitochondria, mitochondrial toxicity, perinatal antiretroviral treatment. 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.