More clinical trials in Africa

“AIDS prevention trial in Zimbabwe targets women
Wed Jul 22, 2009 12:25pm EDT
…
About 5,000 sexually active women are expected to enrol at sites in Zimbabwe, South Africa, Uganda, Zambia and possibly Malawi as part of the study, conducted by the U.S-funded Microbicide Trials Network.
The study will determine whether some of the antiretroviral (ARV) medicines used to treat HIV can also be used to prevent the disease when given as a vaginal microbicide gel or as an oral tablet taken once daily.
In addition, the study, which will specifically test the ARV tablets tenofovir and Truvada, seeks to find out which of the two approaches women would prefer. Tenofovir was also the active ingredient in the vaginal gel.
‘We think its very unique because nobody has really tested the difference between an oral route of prevention compared to a vaginal route of prevention,’ Dr Mike Chirenje, protocol co-chair for the entire study, told Reuters on the sidelines of an AIDS conference. ‘Its not so much which was best, in so much as what would women prefer (to take),’ he said of a study expected to last three and a half years before first results in 2012.
Recent studies have shown that microbicides can protect women — who represent nearly 60 percent of adults living with HIV in the world’s worst affected sub-Saharan Africa region — from catching the virus.”

Those “recent studies” were not cited, however. For a summary of the failures of microbicide research, see “The Research Trough — where lack of progress brings more grants”, 10 September 2008.  Less than a year ago, it had been noted that “two decades of studying microbicides that would block HIV and other sexually transmitted diseases” had led to “several promising candidates that interfere with the process that allows HIV to replicate” — which is far from preventing “infection” in the first place, which is what microbicides or vaccines are intended to do.

What to say about a trial that will feed antiretroviral drugs for 3½ years to 5000 women who are not even “infected”?

For tenofovir (TDF) it is known, for example, that “Renal impairment, manifested by increases in serum creatinine, glycosuria, hypophosphatemia, and acute tubular necrosis, has been reported . . . . In patients who have some degree of pre-existing renal insufficiency . . . tenofovir dosage adjustment is required. However, because no safety and efficacy data that use the dosage adjustment guidelines for renal dysfunction are available, the use of alternative NRTIs (especially abacavir) may be preferred over dose-adjusted tenofovir in this setting” [p. 33, NIH Treatment Guidelines, 3 November 2008]. In addition to renal damage, “adverse events” of TDF include “asthenia [loss of energy], headache, diarrhea, vomiting, flatulence, Fanconi syndrome [a specific form of renal dysfunction], osteopenia [bone loss not yet as severe as osteoporosis]”. Truvada combines TDF with FTC (emtricitabine) which adds the risk of skin discoloration (p. 131).

The popular paraphrase of the Hippocratic Oath, “First, do no harm”, would seem difficult to reconcile with feeding dangerous drugs to healthy human beings when the only conceivable purpose is to find a means of protection that might be an alternative to the entirely non-dangerous use of condoms — leaving aside the fact that there’s not even a sexually transmitted “HIV” to be protected against.

The “science” of AIDS

A Google Alert led me to a very uninformative news item (“Risky sex in Tijuana ups HIV rate”, UPI)   about potentially interesting material having to do with HIV in Tijuana; I was prompted to look at the original article. It’s currently in press at the journal AIDS, and to locate it I had to scan through a list of dozens of articles in press. That reminded me of something I’d long forgotten, how very trivial most of the scientific literature is. One indication of that: the overwhelming majority of research articles are never cited, which makes it exceedingly unlikely that they have been of any use — except for padding a vita for career purposes or for making money for commercial journal publishers whose income derives from advertisements and from “page charges” that authors pay — not personally, of course, but out of their grants. I continue to get invitations to suggest titles for new journals that I might like to edit, the latest one from India mentioning a page-charge rate of $250. In the humanities, it’s called “vanity” publishing when an author has to pay to get into print.

The titles of some of the articles in press in AIDS — accepted for publication, in queue to be printed — suggest why so many publications are never cited, much the same reason as why Senator Proxmire never failed for candidates for his “Golden Fleece” awards satirizing the researches that federal funds supported. The numbers of authors illustrate the career-enhancing purpose of these publications:

“Knowledge of HIV status, sexual risk behaviors and contraceptive need among people living with HIV in Kenya and Malawi” (11 authors)
“The effect of educational attainment and other factors on HIV risk in South African women: results from antenatal surveillance, 2000-2005” (5 authors)
“Comparison of previous and present World Health Organization clinical staging criteria in HIV-infected Malawian children” (11 authors)

Scanning those lists of papers also shows that a number of American researchers have made careers for two decades by doing this sort for research at specific sites in Africa, enthusiastically helped by African colleagues who would otherwise not find it easy to get any research support at all.

But this is a digression from what stimulated this post: several of the articles to be published in AIDS are highly damaging to HIV/AIDS theory, for instance:

Beware antiretrovirals
“Stavudine in antiretroviral therapy: is this the end?” — editorial comment by Kees Brinkman, DOI:10.1097/QAD.0b013e32832d3c5e
“After 1-2 years on HAART, symptoms like lipodystrophy, dyslipidemia, cardiovascular disease, diabetes and lactic acidosis frequently materialized in exposed patients. In particular the development of a stigmatizing lipoatrophy of the arms, legs and face moved many patients to postpone the start of their treatment. . . .  stronger recommendations should be installed not to allow any use of stavudine anymore and to replace stavudine in people currently taking this drug by safer alternatives like abacavir and tenofovir. The longer we wait, the more damage will be done” [emphases added].

It’s not only stavudine, of course, it is all the NRTIs (nucleoside reverse transcriptase inhibitors) whose type specimen is AZT. The November 2008 NIH Treatment Guidelines (Table 9, p. 47) has this very belated statement:

“Monotherapy with NRTI. Single-NRTI therapy does not demonstrate potent and sustained antiviral activity and should not be used” [emphasis in original]

Very belated, because from the introduction of AZT in 1987 until the mid-90s start of the HAART era, that is precisely what “HIV-positive” people and AIDS patients were being subjected to. But, of course, when we “denialists” venture to remark that AZT “treatment” killed several hundred thousand people during that period, the HIV/AIDS groupies deny it.

Perhaps in time the NIH Treatment Guidelines will be warning correctly against ALL antiretroviral drugs even as misinformed and misguided practitioners continue to prescribe them. Just following the statement quoted above comes this:
“Single-drug treatment regimens with a ritonavir-boosted PI, either lopinavir [1] or atazanavir [2], are under investigation with mixed results, and cannot be recommended outside of a clinical trial at this time” [emphasis in original] which would seem to disqualify protease inhibitors as well as NRTIs.

In case the NIH Treatment Guidelines aren’t enough to dissuade anyone from antiretroviral treatment, consider what RxList has to say (updated 3/26/09) about Zerit (stavudine):

Beware antiretrovirals — because THEY KILL
“Non-AIDS-defining deaths and immunodeficiency in the era of combination antiretroviral therapy” (12 authors on behalf of the CASCADE collaboration; only one of the authors declares a conflict of interest, consulting fees from several drug companies; DOI:10.1097/QAD.0b013e32832e9b78).
“Among 9858 patients . . . , 597 died, 333 (55.7%) from non-AIDS-defining causes” — consistent with the NIH Treatment Guidelines (3 November 2008, p. 21):
“In the era of combination antiretroviral therapy, several large observational studies have indicated that the risk of several non-AIDS-defining conditions, including cardiovascular diseases, liver-related events, renal disease, and certain non-AIDS malignancies [14-19] 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.”
The present article confirms also that higher CD4 means lower death-risk, but describes it in this rather peculiar fashion:
“Conclusion: In the cART era, the most frequent non-AIDS-defining causes of death are associated with immunodeficiency, only cardiovascular disease was associated with high viral replication. Avoiding profound and mild immunodeficiency, through earlier initiation of cART, may impact on morbidity and mortality of HIV-infected patients.”
In other words, “non-AIDS” renal and liver failure are now being attributed to immunedeficiency, which is supposed to be caused by “HIV” in “HIV-positive” people, so there’s a justification for starting antiretroviral drugs earlier. Non-AIDS cardiovascular disease is “associated” with “high viral replication”, so that “non-AIDS” disease too can be attributed to the presence of HIV through guilt by association, overlooking as usual that correlation does not prove causation. Thus antiretroviral treatment is being suggested to stave off non-HIV/AIDS ailments?!
I also relish the term “cART”, combination ART instead of highly active ART, reflecting perhaps a belated acknowledgment that it isn’t highly active as well as being deadly.

Use antiretroviral drugs EVEN WHEN THE PROBLEM IS NOT HIV
Here’s another independent instance of recommending antiretroviral drugs to treat non-HIV/AIDS conditions:
“The effect of HAART in 254 consecutive patients with AIDS-related Kaposi’s sarcoma” (9 authors; no conflicts of interest declared, but 3 authors are from Department of HIV Medicine, Chelsea and Westminster Hospital, London, UK; DOI:10.1097/QAD.0b013e32832d080d)
The fact that KS has been ascribed for well over a decade not to HIV but to KSHV or HHV-8 does not prevent talk of “AIDS-related Kaposi’s sarcoma”, because “Recognized as an AIDS-defining illness for over two decades [3], Kaposi’s sarcoma has always been the most common HIV-associated malignancy” — reference [3] being from 1987: MMWR Morb Mortal Wkly Rep 1987; 36 (Suppl 1):1S-15S.
It’s a shame the authors didn’t follow the Kalichman Mandate to ignore publications earlier than 2000 and especially those before 1990 (“Proving HIV/AIDS — Kalichman’s blunders, in a nutshell”, 11 March 2009).

Use antiretroviral drugs even though THEY CAUSE OSTEOPOROSIS
“Continuous antiretroviral therapy decreases bone mineral density” (10 authors, for the INSIGHT SMART Body Composition substudy group; 6 authors declare no conflicts of interest, the other 4 declare many with many drug companies; the primary article was written by two authors, one of them multiple conflicts of interest; DOI:10.1097/QAD.0b013e32832c1792).
Light relief is provided — at least for me — by the penchant for cheery up-beat acronyms like SMART (Strategies for Management of Anti-Retroviral Therapy), even though it might really be “SMARTER” to avoid such therapy. INSIGHT I haven’t yet decoded, but it seems quite popular. For example, I found “International Nifedipine GITS Study Intervention as a Goal in Hypertension Treatment” as well as “Implementing New Strategies with Insulin Glargine for Hyperglycemia Treatment”.

“With continuous ART, BMD [bone mineral density] declined per year by 0.8% (hip), 0.4% (spine), and 2.4% (spine). BMD declined significantly less with intermittent ART. Estimated . . . differences in mean BMD change . . . were 1.4% [hip . . .], 1.3% (spine DXA . . .), and 3.0% (spine qCT . . .). . . . 10 of 2753 participants in the VS [continuous HAART] group and two of 2720 in the DC [intermittent HAART] group reported serious fractures (hazard ratio 4.9 . . .).”
Continuous HAART is associated with a 5-fold greater risk of serious fractures because HAART weakens bones.

Use antiretroviral drugs: they HURT SOME PEOPLE LESS THAN OTHERS
“Risk factors for treatment-limiting toxicities in patients starting nevirapine-containing antiretroviral therapy” (11 authors on behalf of the Nevirapine Toxicity Multicohort Collaboration; DOI:10.1097/QAD.0b013e32832d3b54) 2 authors declare no conflicts of interest. The listing of the various cohorts and their members covers about 3 full pages of the 10½ page article.

The rationale for such a study is rather clear:
“Nevirapine is frequently used as part of combination antiretroviral therapy (cART) regimens . . . for example, to minimize diarrhea or to reduce cardiovascular risks associated with protease inhibitors, to avoid the neuropsychiatric side effects of efavirenz . . . . However, nevirapine is occasionally associated with severe adverse events, typically hypersensitivity reactions that usually occur within the first 18 weeks of treatment . . . . Six to seven percent of patients discontinue the use of nevirapine because of clinically significant hypersensitivity reactions [2–5]. Severe, life-threatening and even fatal cases of hepatotoxicity [6,7] and/or skin rashes [8–10] have occurred in patients taking nevirapine. HIV-1- seronegative adults using nevirapine for postexposure prophylaxis appear at particularly high risk of lifethreatening hepatotoxicity [11]. Among HIV-positive patients, the risk of hypersensitivity reactions is highest in patients with higher CD4 cell counts”.

The conclusions, however, are rather baffling:
“Our results suggest it may be relatively well tolerated to initiate NVPc in antiretroviral-experienced patients with high CD4 cell counts provided there is no detectable viremia”
Perhaps I don’t understand this properly: NVPc (combination nevirapine-based antiretroviral therapy) is relatively well tolerated in patients who have already survived other antiretroviral treatment, provided they have a high CD4 count and no detectable viral load.
It is NOT tolerated even “relatively” well in treatment-naïve patients or those with low CD4 and appreciable viral load.
?So people who are not immune-suppressed and who do not have an active infection can tolerate this antiretroviral drug relatively well. Those people who are immune-deficient and “infected”, and therefore supposedly need treatment, don’t tolerate it?

Use antiretroviral drugs even though THEY CAUSE LEPROSY
“Increased incidence of leprosy following HAART initiation: a manifestation of the immune reconstitution disease” (Research Letter, 8 authors, no declared conflicts of interest; DOI:10.1097/QAD.0b013e32832bb5b7)
Within 3 months of starting HAART, the adjusted hazard ratio for contracting leprosy is 18.5 (1.6-217) at a p value of 0.02, considerably more “significant” than the typically used criterion of p ≤0.05.

Testing antiretroviral drugs
“Randomized, double-blind, placebo-matched, multicenter trial of abacavir/lamivudine or tenofovir/ emtricitabine with lopinavir/ritonavir for initial HIV treatment” (DOI:10.1097/QAD.0b013e32832cbcc2).
Of the 12 authors, only one disclosed no conflict of interest; 6 of them are employees of  Glaxo-Smith-Kline [GSK], which sponsored the study. Another 80 members of the HEAT study team are acknowledged without information about conflicts of interest, plus 21 team members who are employees of Glaxo-Smith-Kline).

Although the article’s title mentions “placebo-matched”, no results are reported that compare drugs to placebo; the two drug regimens are simply compared to one another, and the criterion is “non-inferiority”:
“Primary endpoints were the proportion of patients with HIV-1 RNA below 50 copies/ml at week 48 (missing = failure, switch included analysis) and the proportion of patients experiencing adverse events over 96 weeks. . . . Premature study discontinuation due to adverse events occurred in 6% of patients in both groups. Protocol-defined virologic failure occurred in 14% of patients in both groups.”
In other words, in less than two years, 6% of patients suffered “adverse events” from the drugs, which also failed to suppress “viral load” in 14% of patients.

Detect “recent infections”?
“Performance of an immunoassay at detecting recent infection among reported HIV diagnoses in France, 2003-2007” (DOI:10.1097/QAD.0b013e32832d8754; 7 authors, no declared conflicts of interest)

Testing the CDC-developed STARHS (Serological Testing Algorithm for Recent HIV Seroconversion) on nearly 6800 individuals for whom there was independent information about the time of seroconversion did not confirm an earlier smaller study that had seemed to validate STARHS. Instead, there were marked discrepancies near the 180-day cutoff used to define “recent”, and results varied by geographic origin of the patients, a surrogate marker for sub-type of HIV.
My not-unbiased conclusion: the STARHS test doesn’t do what it’s supposed to.

“HIV” and illness: Which comes first?

According to HIV/AIDS theory, “HIV” — whatever it is that is detected by “HIV” tests — precedes damage to the immune system and consequent illness.

Rethinkers and Skeptics, however, claim the opposite:
According to the Perth Group, “HIV-positive” is merely a symptom of oxidative stress.
According to Duesberg, the presence of “HIV” indicates a condition by which “HIV” is generated as a harmless “passenger” side-effect.
A comparison of “HIV-positive” frequency across population sub-groups indicates that the general state of health or fitness correlates with the tendency to test “HIV-positive”
(The Origin, Persistence and Failings of HIV/AIDS Theory, Figure 22, p. 83)

Specific observations that support the Rethinker view include:
Flu vaccination can lead to a positive “HIV” test
Anti-tetanus likewise
and more such instances in Christine Johnson’s classic enumeration.

A recent article not only adds further confirmation to the Rethinker case, it lends considerable specific support to Tony Lance’s hypothesis that intestinal dysbiosis can lead to testing “HIV-positive”, to dysfunction of the immune system, and to the fungal infections that were the first opportunistic infections described as “AIDS”:
Melinda Wenner, “A cultured response to HIV”, Nature Medicine, 15 (2009) 594-7.

A summary of that article is on-line at TheBody. Have a look at Liang’s comment: “I was very prone to diarrhea and gum infection before being hiv positive.”

In the Nature Medicine article, there’s something similar:
“’It’s almost like the gut is a magnet for the virus early on. [It] becomes compromised in weeks,’ says Bill Critchfield, a postdoctoral fellow at the University of California–Davis.”
A diagnosis of “HIV-positive” will typically follow some signs of illness that led to a doctor’s visit. However, there will rarely or never be any prior knowledge of the condition of the gut. According to the orthodoxy, “HIV” does its work very slowly, not “within weeks”. Ergo: this too is eminently consistent with the hypothesis that damage to the intestinal flora precedes testing “HIV-positive”.
The mainstream has increasingly acknowledged the relation between gut and “HIV”, without yet realizing that this supports the dysbiosis hypothesis and not the HIV/AIDS one.
It’s also worth noting that CD4 counts in the blood continue to be cited by mainstream researchers even as they begin to glimpse that it’s the gut where the action is. As Juliane Sacher (among others) has pointed out, immune-system cells move around the body according to where they’re needed, and the level in the blood cannot be taken as an indication of depletion or increase overall.

Note, too, that when Western sources advocate a natural — dare I say naturopathic? — treatment for “HIV”, in this case probiotic yogurt, it isn’t immediately greeted with cries of “pseudo-science”. That’s reserved for non-Westerners who make similar suggestions and for individuals like Matthias Rath, MD, one-time research colleague of Linus Pauling.

Echt, ersatz, or fake? “HIV” “virions” budding from a cell! Electron micrographed!

AIDS Rethinkers and HIV Skeptics enjoy pointing out that genuine (“echt”) virions of HIV have never been obtained directly from an “HIV-positive” person nor from an AIDS patient, not even in “late-stage” “HIV disease” when those “HIV” virions supposedly reign supreme in massive amounts. The attempted answers that HIV/AIDS groupies come up with tend toward the pitiful.

One of them suggested I look at the NIH website that offers specimens of HIV for researchers to use:
“Is there any reason why you don’t want your readers to know that numerous isolates of HIV are available free of charge at http://www.aidsreagent.org and http://www.nibsc.ac.uk/spotlight/aidsreagent?”

The reason I don’t choose to publicize this, of course, is that these so-called “isolates” are the same old extracts, from cultures in which all sorts of stuff has been mixed together, obtained by taking “bands” of material characterized only by having a density of 1.16 g/ml; and those bands have been shown by electron microscopy to be a motley mixture of all sorts of things (Bess et al., “Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations”, Virology 230 [1997] 134-44; Gluschankof et al., “Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations”, ibid., 230: 125-33). No direct isolation of pure virions from “HIV-positive” people or AIDS patients here.

Others have pointed to electron micrographs of apparently pure “HIV” virions published by Layne et al., Virology 189 [1992] 695-714, perhaps overlooking that paper’s title: “Factors underlying spontaneous inactivation and susceptibility to neutralization of human immunodeficiency virus”. These researchers had synthesized “a molecular clone” of “HIV”. In other words, they put together what they thought an “HIV” genome is and what “HIV” proteins are and created particles of which between 1 in 10,000 and 1 in 10,000,000 were “infectious” — which means only that they could be reproduced by the same culturing process, not that they were capable of actually infecting a human being. Those Frankenstein virions self-destructed with a half-life of 30-40 hours. Anyway, synthesizing isn’t the point; one day we’ll also re-create a woolly mammoth by putting our idea of its genome into a suitable elephant’s egg, or something of the sort, but that won’t make it an echt mammoth. Cloned “HIV” is no substitute for direct isolation of virions from “HIV-positive” people or AIDS patients. If virions have never been found in AIDS patients or “HIV-positive” people, how can we ever know for sure that they actually exist there?

Imagine that you take big magnets and continually sweep them through the junkyards where former automobiles rest. You’ll always bring out the same sorts of certain bits: gears, levers, shock-absorber parts, etc. They’re not all EXACTLY identical, but they have a family resemblance to one another, no matter where the junkyard is; even in other countries, there’ll still be a family resemblance, though it may be of a somewhat different “strain”. You concentrate on what seem to be the universally shared elements, and claim that they come from automobiles that actually exist in those yards in functioning form. Your magnets, goes the claim, are actually detecting intact cars.

Louis Hissink, who has an interesting website that features some unpopular views about cosmology, ancient history, and economics, alerted me to yet another remarkable claim: a series of colored transmission electron micrographs on the National Geographic web-site showing an “HIV” virion actually budding from a cell!

I was surprised that one of the HIV/AIDS groupies had not already dumbfounded me with this conclusive evidence of the veritable existence of echt “HIV”. But then I remembered some of what I used to know about electron microscopy: specimens to be examined by that technique are ultra-thin sections of material “fixed” in some manner to withstand the nearly absolute vacuum that allows electron beams to serve as the “light” source to illuminate the specimen. You can’t do electron microscopy in situ, in vivo. Ergo, those 4 pictures cannot be an echt sequence. Moreover, the odds would be impossibly against capturing such a sequence by preparing a series of specimens: how lucky would you have to be to catch the “budding virus” at just the right moments?

I sent an inquiry to the National Geographic website and was referred to Photo Researchers, who are credited for these images. They responded:

“The photo you listed is represented by our stock agency here in the US. The copyright owner is actually based in Germany and they have many agents selling the piece worldwide.
The only sales we have here in the US have been the Nat. Geo. you linked to and a sale to ‘Junior Scholastic’ back in 2006. Due to the vast distribution of the image there is the distinct possibility that this image has been used in a wide variety of places.”

and

“These are certainly TEM’s [transmission electron micrographs]… but with a few caveats.   First, they have been (obviously) colorized from the original B/W.  Second, this is not a true sequence in that we are not seeing the same virus particle. And third, the cell was repeated in the bottom two frames to create the effect of a sequence.

So I guess in the end they can be considered ‘computer manipulated’ but the base images (virus particles and cell) are true TEM in origin.”

There you have the sort of utterly misleading stuff that’s propagated about HIV/AIDS — no doubt with the best intentions in the world — by people and groups like National Geographic that see themselves as disseminating useful and educational material. In actual fact, images of this sort make the public at large believe that “HIV” has been proven to exist. Just Google “HIV” for “Images” and you can be regaled with a cornucopia of beautifully colored computer-graphic art-work that has no verifiable basis in reality.

Italian analysis of HIV/AIDS data

Professor Ruggiero has provided some additional information about the recent article in Medical Hypotheses that has caused such a furor.

Two videos on Youtube feature discussions of the thesis (Tesi di Laurea) in medicine and surgery by Dr. Mandrioli at the University of Bologna, one of the oldest universities in the world and one of the most prestigious in Italy. The thesis was judged by eleven of the most distinguished Professors of Medicine at Bologna and received maximum marks cum laude (110/110 e Lode). Dr. Mandrioli will be speaking at the Rethinking AIDS Conference in November in Oakland on “Italian epidemiology supports the chemical AIDS theory” [or “drug-AIDS” hypothesis].

http://www.youtube.com/watch?v=7YUoU4EQYAY&eurl=http%3A%2F%2Fwww%2Emarcoruggiero%2Eorg%2Fpapers%2Ehtm&feature=player_embedded

http://www.youtube.com/watch?v=HjvqYRZoBzI&feature=related

Another interesting link is to a blog conducted by a physician, Dr. Fabio Franchi, that is skeptical about HIV/AIDS theory.

http://www.dissensomedico.it/