HIV/AIDS Skepticism

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


Posted by Henry Bauer on 2008/01/19

Clinical trials on human beings are under way to gauge how well tenofovir and emtricitabine protect against HIV infection, with the hope that a regular diet of them could be recommended as prophylaxis.

It’s already known, mind you, that these drugs can produce bone demineralization with chronic use, kidney damage, lactic acidosis (including fatalities), liver damage (including fatalities), and liver cancer. The danger of side effects is greatest when first starting the drugs but also when one stops taking them.

The brilliant idea that this may be useful prophylaxis is based on studies in “humanized” mice—FIVE mice, that is—engineered to have a “human-type” immune system. The media ( help everyone understand how significant this is by pointing out that “Humanized mice . . . have the same immune systems and infection fighting cells as humans”; which could make one wonder why there’s even a need for trials in actual human beings.

The concept of prophylaxis using drugs that treat the actual illness is in itself a remarkable advance. Perhaps instead of exposing babies to the dangers of vaccination, we should simply place them on life-long diets of antibiotics? Come to think of it, we do already practice this sort of prophylaxis by feeding antiretroviral drugs to every available pregnant woman who happens to be HIV-positive—see FIRST: DO NO HARM! (19 December 2007).

As to humanizing mice, I’m sorely tempted to speculate about the possibility of engineering mice to have human-type intelligence—sufficient, at the very least, for carrying on HIV/AIDS research and clinical trials.

* * * * * *

Here is what the Official Treatment Guidelines, December 2007 version, say about the side effects of tenofovir and emtricitabine, which are described in the media story below as “fewer . . . than other HIV treatments”:

“Renal impairment, manifested by increases in serum creatinine, glycosuria, hypophosphatemia, and acute tubular necrosis, has been reported with tenofovir use [152, 153]. The extent of this toxicity is still undefined. . . .
. . . .
Discontinuation of emtricitabine, lamivudine, or tenofovir in patients with hepatitis B coinfection. Patients with hepatitis B coinfection (hepatitis B surface antigen or HBeAg positive) and receiving one or a combination of these NRTIs may experience an exacerbation of hepatitis upon drug discontinuation [164, 165]. If any of the above agents is discontinued, the patients should be closely monitored for exacerbation of hepatitis or for hepatic flare (AII).
. . . .
Need to discontinue emtricitabine, lamivudine, or tenofovir: Monitor clinical course with frequent liver function tests, and consider the use of interferon, adefovir dipivoxil, or telbivudine to prevent flares, especially in patients with marginal hepatic reserve.
. . . .
Pertinent Black Box Warning Information:
Emtricitabine (EMTRIVA); or in combination product with tenofovir DF (TRUVADA) or with tenofovir DF and efavirenz (ATRIPLA):
—Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogues alone or in combination with other antiretrovirals.
—Emtricitabine is not indicated for the treatment of hepatitis B infection (HBV), the safety and efficacy have not been established in patients with HIV/HBV coinfection.
—Severe acute exacerbations of hepatitis B have been reported in patients who discontinued emtricitabine – hepatic function should be monitored closely with both clinical and laboratory follow-up for at least several months after discontinuation of tenofovir in HIV/HBV coinfected patients.
—If appropriate, initiation of anti-HBV therapy may be warranted after discontinuation of tenofovir.
. . . .
Tenofovir (VIREAD); or in combination product with emtricitabine (TRUVADA) or with efavirenz and emtricitabine (ATRIPLA)
—Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogs alone or in combination with other antiretrovirals.
—Tenofovir is not indicated for the treatment of chronic hepatitis B (HBV) infection, safety and efficacy in patients with HIV/HBV coinfection have not been established.
—Severe acute exacerbations of hepatitis B have been reported in patients who discontinued tenofovir – hepatic function should be monitored closely with both clinical and laboratory follow-up for at least several months after discontinuation of tenofovir in HIV/HBV coinfected patients.
—If appropriate, initiation of anti-HBV therapy may be warranted after discontinuation of tenofovir.
. . . .
Studies in monkeys show decreased fetal growth and reduction in fetal bone porosity within two months of starting maternal therapy [371]. Clinical studies in humans (particularly children) show bone demineralization with chronic use; clinical significance unknown [252, 372]. Significant placental passage in humans (cord:maternal blood ratio ~1.0).”

Tenofovir also produces liver cancer in mice.

* * * * * *

Here’s the media report of this study:

“After 25 years of researchers around the globe being confounded by HIV, scientists in Dallas have shown that the virus’s transmission can be stopped with medications. The scientific first, though performed only in lab mice, bodes well for a future when people at high risk for HIV infection would have a convenient way to protect themselves from the virus. . . . experts who have long advocated safe-sex practices are worried that people will seek these drugs without waiting for scientific proof from human studies. . . . One of the drugs, tenofovir, is reportedly being sold at gay dance clubs on both coasts as a protection against HIV. . . .
Someday, people at high risk of HIV infection could be encouraged by doctors to take a daily pill
. . . .
The experiment involved injecting five mice for seven days with two drugs that are commonly used to treat AIDS patients, tenofovir and emtricitabine. On the third day, the mice were inoculated vaginally with HIV, to mimic how most women and girls become infected. ‘Women have no way of protecting themselves from … [sexually transmitted diseases] and HIV,’ said Dr. Garcia, a professor of internal medicine. A preventive medication ‘would empower them to at least have a fighting chance.’ . . .
An important step toward the current UT Southwestern study was Dr. Garcia’s 2006 development of a mouse that had been made susceptible to HIV via transplantation of a ‘humanized’ immune system’. . . .
The two [drugs] . . . have fewer side effects than other HIV treatments. The two drugs are part of several studies in people, funded by the U.S. government, that are testing safety and effectiveness in preventing HIV infection among intravenous drug abusers, young men and women who are sexually active and men who have sex with men. Test sites include San Francisco, Atlanta, Botswana, Thailand, Peru and Ecuador” [emphases added].
(“Dallas scientists stop HIV from spreading in mice—Experts caution that Dallas team’s findings were only in mice”, by Sue Goetinck Ambrose & Sherry Jacobson , Dallas Morning News, 15 January 2008).
The source article is “Antiretroviral pre-exposure prophylaxis prevents vaginal transmission of HIV-1 in humanized BLT mice” by Denton et al., PLoS Medicine 5 #1, e16 doi:10.1371/journal.pmed.0050016 in PLoS Medicine


  1. Brian Carter said


    I’ve had a couple of complete non-responses from guys taking these chemotherapy for years, whom I shared information similar to yours here. Their attitude is, “Yea, so what”. They’ve obviously developed a deep mental block and although they feel like shit day in and day out, they keep going back for prescription after prescription. It is my theory that these regimens manifest psychiatric delusions from induced neurological damage making it ever more hard for them to see just how badly they’re skewing their life up. Moral of the story: “You can lead a horse to water but you can’t make them drink.”

  2. hhbauer said

    You may well have a point, I’ve seen mentions of “HIV-related” dementia and neurological symptoms which—like “HIV lipodystrophy”—I take to be “side” effects of the drugs, not of the “HIV”.

    But one should not discount the real dilemma such people as you describe find themselves in. Are they to take medical advice from their doctors or from amateurs?! Let’s say they see something in what you’re saying, but on the other hand they find it hard to believe that their doctors aren’t aware of all this. How to decide??

    I think many of us face this sort of dilemma in a much milder, not life-threatening form, when our doctor prescribes something about which we have doubts—and don’t many of us have justifiable doubts about almost ANY medication?

    One person who found my book very convincing, and has shared it with others including his doctors, had started HAART not long before he saw the book. He was feeling better after the treatment started. His doctor is keeping him on low doses. How could he decide to stop the treatment altogether, which also means changing doctors?

    There must be quite a lot of people who are in that very real, tragic, dilemma. That won’t end until the HIV/AIDS dogma is officially concluded so that well-meaning physicians no longer advise antiretroviral treatment.

    Among the points that dissidents need to address is, why do some people feel better after starting HAART? Some suggestions have been made—antimicrobial action of the drugs, placebo effect—but we need something more than suggestions to be really convincing.

  3. CathyVM said

    Surely the bigger the intervention the bigger the placebo effect? I remember the old wives’ tale that the nastier the medicine tasted, the more potent it was. Combine these two phenomena together and it may just be stronger than the nocebo death sentence bone-point that would most certainly decimate any sense of health.

  4. hhbauer said

    I’m not sure what you mean by “bigger” intervention. If it means more physiologically potent drugs, then it’s less likely that placebo could overcome their toxicity.

    I don’t think the factors that influence strength of the placebo response are well understood. Excellent discussions are in Howard Brody, “The placebo response”; Shapiro and Shapiro, “The powerful placebo”; Ann Harrington (ed.), “The placebo effect”.

  5. CathyVM said

    An orthopaedic surgeon was challenged by one of his nurses in 1996 on this issue. The nurse argued the bigger then intervention, the bigger the placebo effect, and what bigger intervention than going under the surgeon’s knife? First they did a small pilot study and later a much bigger RCT with 180 knee OA [osteoarthritic] patients undergoing arthroscopic debridement, lavage or placebo (they gave them a GA [general anesthetic] and made 2 small incisions only). There was no difference between the groups in outcomes [1]. So is debridement of OA knees useless, or is placebo treatment effective in debriding knees? Apparently the Japanese have beliefs that the size, colour and even shape of tablets affect the potency of the medicine (sorry no citation – it was a marketing report). Clomipramine and placebo worked equally well in reducing aggression in dogs [2]. How does the dog know he’s supposed to feel better? The placebo/nocebo effect is endlessly fascinating. Who knows, perhaps the toxicities of HAART themselves have some kind of strong placebo effect of their own – “Hey they make me feel like crud so they must be powerful drugs.”
    1. Moseley, J.B., et al., A controlled trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med, 2002. 347(2): p. 81-8.
    2. White, M.M., et al., Effects of clomipramine hydrochloride on dominance-related aggression in dogs. J Am Vet Med Assoc, 1999. 215(9): p. 1288-91.

  6. hhbauer said

    Yes indeed, CathyVM, “The placebo/nocebo effect is endlessly fascinating”. One of those books I recommended, can’t recall which one, gives another example of surgery that was later found to be successful only as a result of placebo. The interpretation was that surgery induces a very strong conviction that it will work, thereby triggering the placebo response.

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