AIDS AS INTESTINAL DYSBIOSIS

The article by Tony Lance posted in WHAT REALLY CAUSED AIDS . . . [20 February 2008] is powerfully persuasive that the outbreaks of “AIDS” in the 1980s were really outbreaks of intestinal dysbiosis among people whose lifestyle was conducive to such dysbiosis. It is further support for Lance’s thesis that some doctors have been successfully treating “AIDS” patients for intestinal dysbiosis, or something very like it, from the very beginning of the “epidemic”.

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Dissenters from orthodox HIV/AIDS theory differ among themselves over what really caused AIDS. John Scythes, for example, believes that undiagnosed syphilis played and perhaps continues to play a significant role (for details, see the website maintained by his colleague Colman Jones ). But Scythes doesn’t claim to have all the answers, and he was an outstandingly objective and helpful reader of drafts of my book. He has met a number of people in various parts of the world who are involved in HIV/AIDS in one way or another, and recently he mentioned to me Dr. Juliane Sacher in Germany as someone who has successfully treated “AIDS” patients without resort to antiretrovirals. I asked Dr. Sacher for published accounts of her work, and she sent me 3 articles published in 2006 in the German periodical Raum & Zeit (141: 34-38: AIDS—Chronology of the mistakes; 142: 18-23: II. AIDS—The virus that doesn’t exist; III. 143: 60-62: “AIDS”—How alternative therapies can help [titles translated by Henry Bauer]). It turns out that Dr. Sacher’s practical clinical experience with AIDS patients and with HIV-positive people affords convincing support for Tony Lance’s hypothesis of intestinal dysbiosis.

Sacher had served as a physician with Lufthansa and had noted already in the 1970s that male flight-crews often had reduced lymphocyte counts, were often homosexual, and indeed were among the first AIDS cases in Germany. In the 1980s, Sacher was in a medical group in Frankfurt that treated many AIDS patients, and she noted their high, sometimes extreme levels of immunoglobulins and antibodies: from 35 to 40 or 45% as against the normal 18%. But T4-cells, which HIV supposedly destroys, are instrumental in the production by B-cells of these globulins; so how could patients supposedly low in T4-cells be producing excess globulins? The answer, shown by research in the early 1990s, is that the low counts of T4-cells in the blood, characteristic of AIDS, does not mark destruction of those cells but rather reflects that they move elsewhere—in particular, into the lymph system. They act against inflammation of the lymph nodes, and return into the blood once the inflammation subsides.

Sacher also notes that the balance between two types of T4 cells is shifted in AIDS patients: typically they display a relative dearth of Th1 and an excess of Th2 cells.
In 1987, Germany funded research to asses the efficacy of antiretroviral treatment of AIDS patients. Dr. Sacher had the largest or second-largest group of HIV/AIDS patients in Germany enrolled in the study. Results after one year showed that in patients treated with AZT the T4-cell counts had decreased by 70%, whereas in those treated by Sacher using alternative treatments–80-90% of all her patients–the decrease had been an average of only 7.5%! Most of these patients had had full-blown AIDS, though a few were HIV-positive but asymptomatic. This result was described in the Ärzte-Zeitung (Physicians Newsletter), 6/7 October 1989, #189, page 15: some 50 patients treated by alternative means did better than 56 patients treated with AZT (Sacher’s Raum & Zeit article no. I includes a photocopy of that publication in the Ärzte-Zeitung).

Sacher’s “alternative” approach to treatment of AIDS patients is informed by the views of Dr. Heinrich Kremer; his 2005 book, “Die stille Revolution von Krebs- und AIDS-Medizin” (The quiet revolution in cancer and AIDS medicine), Ehlers Verlag, Wolfratshausen, is to appear in English translation in the near future. The key is recognition that glutathione is a most important antioxidant which also regulates the Th1/Th2 balance: deficiency of glutathione shifts the balance in the direction of Th2. HIV-positive patients invariably have a glutathione deficiency, and their health improves when this is rectified. In addition, Dr. Sacher monitors carefully and corrects deficiencies in vitamins and minerals; she encourages a healthy lifestyle—exercise, minimizing stress—and uses a number of dietary supplements as indicated in individual cases.

In Part III of her articles in Raum & Zeit, Sacher offers more details of how she treats specific conditions that AIDS patients often experience—diarrhea, bronchitis, bladder and kidney problems. She also recommends preventive measures including specific laboratory tests. A brief professional biography of Dr. Sacher is included in these articles:
Dr. Sacher has been in private medical practice since 1983. She worked with the German Federal HIV Study between 1987 and 1993; served in 1988 on the Parliamentary HIV/AIDS Commission; and was co-recipient in 1990 of a prize of 100,000 Deutschmark for her work with HIV/AIDS patients. Between 1975 and 1993 she served under contract with Lufthansa. From 2000 to 2002 she worked part-time in the biostatistics unit of Wuppertal University. She takes a special interest in all aspects of chronic illnesses, and in complementary as well as mainstream medicine.

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I’ve often been struck by how frequently I come across, “by chance” or from unexpected quarters, material relevant to what I’m thinking about at some given moment. Here it is again. Dr. Sacher’s clinical experience with “AIDS” patients is fully in line with Tony Lance’s intestinal-dysbiosis theory, in particular the role of glutathione and of Th1-Th2 shifts. Dr. Sacher’s work shows the salience of those factors; Lance’s theory explains why so notable a proportion of gay men display glutathione deficiency and Th1/Th2 imbalance and therefore benefit from Dr. Sacher’s approach to medical care.

WHAT REALLY CAUSED AIDS: SLICING THROUGH THE GORDIAN KNOT

The hypothesis that HIV causes AIDS fails to explain the demographic characteristics of HIV-positive tests (The Origins, Persistence and Failings of HIV/AIDS Theory); it has generated a large number of conundrums and claims that cannot be reproduced (for example, as to herpes, circumcision, vaccines—see HERPES AND HIV, 8 February 2008). Virions of HIV have never been isolated from HIV-positive people. Nor has the hypothesis led to satisfactory answers to salient questions:
1. Why did AIDS appear first among gay men in the United States?
2. Why in the late 1970s to early 1980s?
3. Why did it manifest in the specific forms of Pneumocystis carinii pneumonia, candidiasis, lymphadenopathy, and Kaposi’s sarcoma?

Dissent from HIV/AIDS theory has persisted for some two decades, but the dissidents agree only over the inadequacy of that theory; no consensus has formed over a possible alternative among a number of suggestions: drug abuse; multifactorial—a combination of many insults including a variety of infections and antibiotic treatments; undiagnosed syphilis. None of those offer convincing answers to those three questions. And dissidents have an additional question to answer:
4. If HIV doesn’t cause AIDS, why do antiretroviral drugs sometimes make people feel much better, quite quickly? (even if that benefit doesn’t last, and the drugs themselves cause harm in the longer run).

Drug abuse evidently has something to do with AIDS.
John Lauritsen was first to point out that all the early AIDS patients had a history of using “recreational” drugs and that the Centers for Disease Control and Prevention obscured the fact through its misguided “hierarchical” classification of AIDS cases. Lauritsen also argued cogently for nitrites, “poppers”, as the specific cause of Kaposi’s sarcoma (http://paganpressbooks.com/jpl/POPPERS.HTM).
Peter Duesberg has gathered considerable supporting evidence for the role of drug abuse, including different manifest infections associated with different drugs .
Still, acknowledging an association with drug abuse leaves unanswered those same three questions. After all, there had been an epidemic of drug abuse, not restricted to gay men, in the 1960s to 1970s. Then, and also in more recent times with cocaine, crack, and meth, certain consequences deleterious to health are well known—but they did and do not prominently feature Pneumocystis carinii pneumonia or candidiasis.

The multifactorial hypothesis, too, lacks convincing answers for the specificity of the affected group, when it was affected, and what the manifest infections were.

The inability to offer good explanations for these specifics may well be a major reason why the dissidents’ sound arguments against HIV/AIDS theory have been so little attended to. It’s one thing to show that some theory is inadequate, but it’s a well known aspect of science that an unsatisfactory theory is not abandoned until a better alternative becomes available. Non-scientists, too, can only shrug helplessly when they are shown how obvious the evidence is that HIV doesn’t cause AIDS; they need, quite reasonably, to be given at least plausible answers for what caused AIDS and what “HIV” is.

After my book was published, I learned a great deal more from people who got in touch with me, and yet more after I began writing this blog. The most striking discussion that was new to me, something that gave me a “Eureka” moment, came from Tony Lance, whose explanations offer satisfactory answers to all four of those central questions. What we now know as “AIDS” had been described at first as “GRID”: Gay-Related Immune Deficiency. It turns out that it should have been named Gay-Related Intestinal Dysbiosis:

gay-relatedintestinaldysbiosis.pdf

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