HIV/AIDS Skepticism

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


Posted by Henry Bauer on 2008/02/25

In AIDS AS INTESTINAL DYSBIOSIS (23 February 2008), I mentioned that the clinical experience of Dr. Juliane Sacher in Frankfurt, Germany, is entirely consistent with Tony Lance’s identification of intestinal dysbiosis as a likely cause of testing HIV+ and also of suffering AIDS, especially among gay men who indulge in certain practices.I’ve been asked for English versions of the German articles that Dr. Sacher had sent me. Here is a free translation of them, abbreviated where material could be omitted without changing the meaning.



  1. cytotalker said

    May I direct you toward Ray Peat’s essay on immune deficiency, which is centered on endocrinology, and which I would consider indispensable. There is much about physiology and metabolism that escapes the physician but which is clear to the biologist. I hope you find this insightful.

  2. cytotalker said

    Do excuse the following voluminous post.

    Little known and amazing as it may seem is that aspirin therapy actually outperforms HAART in immune reconstitution.

    HAART is not as successful as it is hyped to be. Progress with HAART is exuberant the first four months and dwindles afterwards, and reaches a plateau after three years with many patients never attaining a CD4 count sufficient to overcome immune deficiency.
    (registration required)


    Methods: A total of 1281 HIV-infected patients initiating HAART were enrolled in the AntiPROtease (APROCO) cohort. We investigated determinants of increase in CD4 count using longitudinal mixed models in patients who maintained a plasma HIV RNA
    Results: A total of 870 patients had a virological response at month 4. The median follow-up time was 57 months. Mean estimated increases in CD4 count in patients with persistent virological response were 29.9 cells/µL/month before month 4, 6.4 cells/µL/month between months 4 and 36, and 0.7 cells/µL/month (not significantly different from 0) after month 36. Three factors were associated with a significantly positive CD4 count slope after month 36: male gender (+0.9), no history of antiretroviral therapy at baseline (+1.7) and baseline CD4 count 500 cells/µL was achieved in 83% of those with a baseline CD4 count ≥200 cells/µL and in 45% of those with a baseline CD4 count
    Conclusion: The increase in CD4 count reaches a plateau after 3 years of virological response. Even if patients initiating HAART with low CD4 counts still show a CD4 count increase after 3 years, it remains insufficient to overcome immune deficiency in all patients.

    It turns out that the initial HAART-induced CD4 boost is actually due to mere lymphocyte redistribution.

    These data provide evidence suggesting that initial increases in blood CD4+ cell counts on HAART are due to redistribution and that this redistribution is mediated by resolution of the immune activation that had sequestered T cells within lymphoid tissues.

    This “resolution of immune activation” is due to protease inhibitors hijacking the immune activation process via mechanisms totally unrelated to viral control. They will modify immune activation even in HIV seronegatives.

    The HIV protease inhibitor Indinavir inhibits cell-cycle progression in vitro in lymphocytes of HIV-infected and uninfected individuals

    It is concluded that IDV may prolong cell survival indirectly by inhibiting their entry into cell cycle. In individuals on PI therapy, PI-mediated effects could potentially modulate immunologic responses independently of antiviral activity against HIV.

    It is no longer controversial to state this in orthodox research circles, since viral cytotoxicity has been discarded even among the most orthodox researchers such as David Ho and chronic immune activation is the accepted paradigm.

    Meanwhile, doctors and public education continue to feed the public with the virus-kills-lymphocyte fallacy together with the misperception that HAART’s immune restoration is effective and that it is due to viral control.

    There are short-term benefits to HAART. For instance, ritonavir is an effective KS treatment independent of its viral control effect.

    Transcriptional activation of nuclear factor-B, as induced by the KS-promoting factor TNF-, the HIV-1 Tat protein, or the human herpesvirus 8 protein ORF74, was inhibited by ritonavir. KS-derived cell lines underwent apoptosis in vitro after treatment with ritonavir at concentrations that are obtained in clinical therapy (3-15 µM). In a KS mouse xenotransplantation model, ritonavir inhibited tumor formation and progression by KS-derived cells. Taken together, these data suggest that ritonavir has antineoplastic effects that are independent from its ability to inhibit the HIV protease.

    However, TNF, nuclear factor-B are effectively controlled with aspirin and other NSAIDs, but aspirin has repeatedly been shown to be of higher therapeutic value while offering benefits which oppose the toxicities of HAART.

    In the aspirin treated group, the CD4 count increased by 23.3% from a mean baseline of 363 after 24 weeks [p=0.0]5] to 665 after 36 weeks [p=0.078 by the Wilcoxon rank test] followed by a statistically insignificant drop to 495 after 12 months. During the 52-weeks of aspirin treatment, the overall mean CD4 count increased from 363 to 495 [p=0.03].

    Impressive as this is, the most important finding is that

    All the patients who were p24 antigen positive at enrolment became p24Ag negative after 6 months in the aspirin arm.

    Who would have thought, control the inflammation and the body heals itself.

    Layman humanitarian Howard Armistead has done much homework researching the biomedical archives, speaking at reputable AIDS conferences and has been promoting SAM (Selenium, Aspirin, Multivitamin) therapy in Africa for many years with much success, oftentimes out of his own pocket. His work is admirable. He writes:

    In conclusion, comparing their peak increase in CD4 cells, ASA has been shown to increase CD4 more than twice as much as AZT and is better able to sustain this increase. At the one-year point, while the CD4 count of those on AZT monotherapy decreased 25% below baseline levels, those taking aspirin maintained an average 35% increase in CD4. This reflects the fact that aspirin possesses not only anti-retroviral activity as an NF-κB inhibitor, but it can also increase immune function, again through inhibition of NF-κB.

    The rest of his website is filled with gems such as this one.

    It is so mind boggling that few would take it seriously.

    Ray Peat discusses and documents aspirin therapy’s powerful role in cancer, heart disease, alzheimers, and other degenerative disease and the disinformation by industry to cloud these facts.

    The common factor to all these disease, inflammation and excitotoxicity, TNF (Tumor Necrosis Factor), prostaglandins, and NF kappa B.

    For anyone who peruses the biomedical research, none of this is even controversial.

  3. hhbauer said


    Many thanks for this informative comment. (For some reason it was in my SPAM folder, and I don’t know how long it’s been there.)

    That CD4 counts in the blood decrease through re-distribution in the body, and that counts rebound once inflammation has been taken care of, are consistent with some of the points made by Dr. Juliane Sacher and for which I didn’t yet have sources, so I’m very glad to have the citations you list.

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