HIV/AIDS Skepticism

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The Lazarus Effect and the puzzle of delayed illness in “HIV-positive” gay men

Posted by Henry Bauer on 2014/05/06

Recent comments from CJ and some digging into the past (Reminiscing; not much new under the sun; why gay men and Africans are the predominant victims) brought to the forefront of my mind what has been lurking in the background for quite a long time, the puzzle that is of literally vital importance to some unknown number of gay men: those who are aware of the lack of proof that HIV causes AIDS, who are both “HIV-positive” and healthy for a long time, but who then suffer illness which, for one reason or another, is ascribed or ascribable to “HIV”.

The evidence that HIV does not cause immunedeficiency and AIDS is powerfully strong in a number of ways (The Case against HIV). What first convinced me personally was the accumulated data on “HIV-positive” tests: what those tests detected is neither infectious nor correlated with AIDS (The Origin, Persistence and Failings of HIV/AIDS Theory).
But that is overall. Could some small proportion of all the cases nevertheless conform to the mainstream view? Is it possible that HIV is after all what the mainstream says it is, but is responsible for only a small proportion of AIDS cases?
That seems awfully unlikely. Similar arguments apply as against the possibility that data from “HIV-positive” tests might be invalidated by contamination of samples or false positives (p. 39 ff. in The Origin, Persistence and Failings of HIV/AIDS Theory): the data show extraordinary regularities with respect to sex, age, and race, at all levels of average “HIV-positive” prevalence. There seems no room for a “real HIV” to be lurking in the mass of mistaken “HIV”: if there were, then one or more of those correlations should break down at low prevalence.
Further: Everything the mainstream says about HIV has turned out to be wrong: that it targets T-cells and somehow destroys them indirectly by some occult mechanism, that it’s sexually transmitted, that it hides somewhere during a latent period of a decade or so.

So it seems impossible that the mainstream view could be valid in a tiny proportion of all instances when it is definitely wrong in almost all cases.

If Duesberg is right and HIV is a “passenger” virus, could it be almost always harmless as Duesberg claims and yet harmful to some people some of the time?
If de Harven is right and “HIV” tests pick up circulating DNA and things from endogenous retroviruses (HERVs), could one of those HERVs occasionally become functional, active, harmful?

Such speculations seem unlikely to be true. What an astounding coincidence it would be that everything the mainstream claims has been shown to be unfounded or ill-founded in innumerable instances and yet could be correct in a tiny proportion of instances, so tiny that all the observed correlations are not significantly affected.
I can’t see it.

Doesn’t the lifesaving cART or HAART demonstrate that the mainstream is basically correct?
Not at all. Antiretroviral drugs are not life-saving (Section 7.1.3 in The Case against HIV), indeed the drugs are incredibly toxic. That mortality rates declined almost immediately when HAART was introduced showed not that HAART is good but that it is not as highly toxic as what it replaced (Section 5.1.6 in The Case against HIV).
Moreover, what HAART replaced continues in use, albeit in lower doses, within HAART. Components of that — AZT and its cognate NRTIs and probably NNRTIs and the other kinds of antiretroviral drugs — destroy bone marrow and mitochondria (among other nasty effects) to produce long-term, cumulative, damage, albeit perhaps so gradually that consumers might live for quite a long time, though uncomfortably and in increasingly fragile health.

The Lazarus Effect is hyped by mainstream propagandists as proof that antiretroviral drugs work and transform illness into health: there have been a number of anecdotal accounts over the years of people seriously ill with “AIDS” rising vigorously from their sick-beds within a day or two of starting antiretroviral drugs.
But the Lazarus Effect actually speaks against HIV/AIDS theory, not for it.
HIV is not claimed to cause any direct harm (Section 1.3 in The Case against HIV), only indirectly by supposedly destroying the immune system and allowing opportunistic infections to get a foothold. Antiretroviral drugs are designed to prevent replication of HIV, and there is no reason to expect that such an effect could bring rapid recovery from an illness. Rather, the “antiretroviral” is evidently acting against whatever opportunistic infection or inflammation a somehow weakened immune system allowed. Antiretroviral drugs are known to be magnificently toxic to living cells, and the Lazarus Effect actually demonstrates the antibiotic action of “antiretroviral” drugs. As Drs. Koehnlein and Sacher have pointed out, this gives grounds for prescribing antiretroviral drugs for short periods when it has not been possible to identify the specific cause of an illness. In no way does the Lazarus Effect support HIV/AIDS theory or the use of antiretroviral treatment over extended periods of time (let alone for so-called pre-exposure prevention, PrEP — see Poisonous “prophylaxis”: PrEP [Pre-Exposure Prevention]).

Mainstream shibboleths in relatively recent times have come to include the presumption that “HIV” can somehow cause damage directly to organs including the brain: publications refer to “HIV-associated” dementia, lipodystrophy, arthritis, and more. But those ailments have been “HIV-associated” only since the advent of antiretroviral treatment, and they are actually caused by the antiretroviral drugs (Section 4.3.4 in The Case against HIV); those drugs have legions of toxic effects and are anything but “life-saving” (Section 5 in The Case against HIV).

Another possible explanation for the Lazarus Effect is hormesis: Substances and types of radiation that are harmful at larger doses may actually be beneficial at low doses — the dose-response curve is U- or J-shaped. Thus an initial or short-term “antiretroviral” treatment might appear as life-saving. A common explanation for hormesis is that the poisonous stimulus brings the immune system into action to a degree that more than outweighs the poisonous effect.
The phenomenon of hormesis has been controversial, but it is being increasingly recognized as genuine. A useful review is “Defining hormesis” by Calabrese and Baldwin (Human & Experimental Toxicology, 21 [2002] 91-7 ). A specialist society is dedicated to the study of hormesis: the International Dose-Rresponse Society  which has published a journal for more than a decade.

A personal speculation: some of the adjuvants used in vaccines might work because of hormesis since such adjuvants as squalene and aluminum salts have been reported as harmful at large doses.

* * * * * * * *

How then to comprehend cases of gay men who have been both “HIV-positive” and healthy for a long time and who then suffer illness which, for one reason or another, is ascribed or ascribable to “HIV”?

Taking the dissident stance that “HIV” is not the cause of immunedeficiency, one recalls that there are innumerable possible cause for immunedeficiency (described comprehensively by Root-Bernstein in Rethinking AIDS—The Tragic Cost of Premature Consensus, Free Press, 1993).
Furthermore, it is not only “HIV-positive” gay men who experience illness that their doctors cannot diagnose specifically (When doctors can’t tell you what’s wrong).  It is not impossible, after all, that when gay “HIV-positive” men become ill, that the illness has nothing to do with being gay or with being “HIV-positive”. As we go through life, all of us — women and men, heterosexual and bisexual and homosexual — sooner or later lose health and die.

Still, there is at least one reason why “HIV-positive” gay men may be especially prone to illness: the Nocebo Effect.
It has become generally understood that the Placebo Effect is very real, albeit its mechanism is not understood: Belief that one is being cured can in itself effect a cure *.
It is less widely understood that the same not-understood mechanism can have the opposite, nocebo, effect: Belief that one is going to become ill or to die can in itself bring about illness or death. Not widely enough understood, especially by doctors, is that what a doctor says to a patient can be very damaging when the doctor is simply trying to be straightforward and truthful about conveying bad news **.
This is clearly of great relevance with “HIV/AIDS”, as discussed in The AIDS Cult by John Lauritsen & Ian Young (ASKLEPIOS, 1997), and is clearly pertinent to the puzzle of “HIV-positive” gay men who consider themselves HIV/AIDS dissidents and have been healthy for a long time but then become ill with symptoms associated with AIDS.
It cannot be easy to thoroughly believe the dissident view if one is not a doctor or scientist widely read in the copious technical literature. Most gay men surely find themselves in the dilemma of having to choose who to believe, mainstream doctors and scientists or dissident doctors and scientists. It cannot be easy, when one’s own health and life are at stake, to make such a choice, to believe one group or the other without fully understanding the technical issues, having to take opinions on faith by trusting the expertise and honesty of people who are not known on a personal level.
Surely most gay dissidents have at least occasional doubts, perhaps only subconscious, that perhaps the mainstream could be right after all. That sort of doubting, worrying, would be prime ground for generating stress and a nocebo effect.

* * * * * * * *

This is an attempt to clarify the dreadful dilemma faced by some number of gay men.
In recent correspondence made available for wider distribution, one man in this situation wrote that antiretroviral drugs were effectively treating his cytomegalovirus and toxoplasmosis, at the cost of such “side” effects as : nausea, pain / headache (to the point of continual moaning and pacing), itchy groin/feet (scratched until I bled), insomnia, fatigue, bags under my eyes, bloated, swollen ankles, calves and thighs, diarrhoea, tingling hands, feeling cold”.
The fundamental unresolved problem is how to strengthen a weakened immune system, and medical science seems to offer no help in that direction: “I’ll wean myself off the medications over the coming year, but getting my immune system (specifically my cell-mediated immunity) operating well has been problematic. Let’s see if I succeed the third time around!”.
Dr. Christian Fiala commented that antiretroviral drugs are certainly effective against bacteria, more so than regular antibiotics, and also against viruses, “However you have to be careful that they kill the virus before they kill the patient”. Dr. Claus Köhnlein emphasized that antiretroviral drugs can be useful in extreme cases, but “HIV theory is still the reason for a massive overtreatment because most patients are being treated prophylactically”.

Clarification is needed, I believe; but what’s really needed is help in finding ways to strengthen immunity and to diagnose the actual underlying cause of the weakened immunity in each of these individual cases. That’s where research is needed most desperately.
* Howard Brody with Daralyn Brody, The Placebo Response: How You Can Release the Body’s Inner Pharmacy for Better Health (Harper Perennial, 2001); Arthur K. Shapiro and Elaine Shapiro, The Powerful Placebo: From Ancient Priest to Modern Physician (Johns Hopkins University Press, 2000); Anne Harrington (ed.), The Placebo Effect: An Interdisciplinary Exploration (Harvard University Press, 1997).
** For a review of studies, see Nocebo phenomena in medicine: Their relevance in everyday clinical practice by Winfried Häuser, Ernil Hansen, & Paul Enck, Deutsches Ärzteblatt International, 109 (2012) 459-65 (in English).  The Skeptic’s Dictionary gives a useful summary (nocebo and nocebo effect). A few anecdotes are cogently recounted on YouTube by Helen Pilcher (The nocebo effect — Helen Pilcher — nothing event).

Posted in Alternative AIDS treatments, antiretroviral drugs, HIV as stress, HIV does not cause AIDS, HIV risk groups, HIV skepticism, HIV/AIDS numbers | Tagged: , , | 24 Comments »

Holy Grails, Unicorns, and HIV Vaccines

Posted by Henry Bauer on 2013/08/22

The three subjects of my title have these things in common:

1. No one can produce an authentic specimen.
2. All the evidence for their existence is anecdotal and based on human testimony.
3. Dedicated and ingenious quests have failed to locate an authentic specimen.
4. Nevertheless, their existence is attested by a cult of true believers.

These commonalities occurred to me as I was rummaging in my old files and became rather surprised at the number of mentions of HIV vaccines: new clues for what could lead to a vaccine; promising breakthroughs in understanding how to construct a vaccine; grants from private and public agencies for research on vaccines; organizations set up to facilitate cooperative work toward a vaccine; clinical trials of potential vaccines — and failure after failure after failure. Here is just a small sample from my randomly gathered files:

1984: Vaccine probably within a couple of years
—— Robert Gallo: “Oh, possibly in a couple of years”, cited at p. 176 in Great Feuds in Medicine by Hal Hellman (Wiley, 2002);
—— Margaret Heckler, 23 April press conference: “We hope to have such a vaccine ready for testing in about two years”, cited at p. 25 in The AIDS Bureaucracy by Sandra Panem (Harvard University Press, 1988); at p. 64 in AIDS at 30: A History by Victoria A. Harden (Potomac Books, 2012).

1985: “Recent demonstrations of neutralizing antibodies in AIDS and pre-AIDS patients . . . are encouraging for the prospects of a vaccine”
—— Wong-Staal & Gallo, “Human T-lymphotropic retroviruses”, Nature, 317 (1985) 395-403.

But 10 years later, no success and not even any obvious advance:
1995: However, “Nobody can say the data were encouraging. It’s all smoke and mirrors. There’s nothing there”, according to AIDS vaccine researcher John P. Moore
—— Jon Cohen, Shots in the Dark: The Wayward Search for an AIDS Vaccine (Norton, 2001), p. 275.

1999: Elite controllers of HIV could lead to vaccine development
—— Sarah Rowland-Jones, “Long-term non-progression in HIV infection: Clinico pathological issues”, Journal of Infection, 38 (1999) 67-70.
—— Philippa J. Easterbrook, “Long-term non-progression in HIV infection: definitions and epidemiological issues”, Journal of Infection, 38 (1999) 71-3.

1999: “Promising results for Vical’s HIV vaccine”
—— New Statesman, 30 November 1999.
By 2007, not so promising: “NIH determined that it would not conduct the PAVE 100 study”.
—— Vical, “HIV Vaccine”.

2005: “[D]evelopment of an HIV vaccine remains one of the most difficult challenges confronting biomedical research today”
—— Coordinating Committee of the Global HIV/AIDS Vaccine Enterprise, “The Global HIV/AIDS Vaccine Enterprise: Scientific Strategic Plan”, PLoS Medicine, 2 #2 (2005) e25, pp. 0111-0121.

2006: “[A]bout 2,000 . . . controllers worldwide whose entire genetic makeups will be carefully examined by an international team of scientists as part of the quest to discover an AIDS vaccine”
—— Warren King, “Rod Fichter has lived with HIV for 20 years with no symptoms”, Seattle Times, 23 November 2006.

2006: “As many as one in 300 HIV patients never get sick . . . . their cases can help in the search for a vaccine”
—— Maggie Fox, “ ‘Elite’ HIV patients mystify doctors”, Reuters, 16 August 2006;

2006: Elite controllers of HIV could lead to vaccine development (cf. 1999).
—— Marmor et al., “Resistance to HIV Infection”, J. Urban Health, 83 (2006) 5-17.

2006: “Swedish prime-boost HIV DNA vaccine shows strong responses”
—— Keith Alcorn, 1 September 2006;, accessed 23 September 2006 (broken link).

2006: “Is an AIDS vaccine possible? Experts more optimistic after annual vaccine meeting”
—— Keith Alcorn, 5 September 2006;, accessed 23 September 2006 (broken link).

2007: “[W]ill help with the design of an HIV vaccine”
—— “Novel genetics research advances possibility of HIV vaccine”,, 8 July 2007; .

2007: Elite controllers of HIV could lead to vaccine development (cf. 1999)
—— O. J. Fagbire, “Elite controllers of HIV could lead to vaccine development”, 10 June 2007;, accessed 21 June 2007 (broken link).

2007: But immune response to one strain of “HIV” may not protect against other strains
—— Piantadosi et al., “Chronic HIV-1 infection frequently fails to protect against superinfection”, PLoS Pathog, 3 (2007) e177.

2007: “Ending of HIV vaccine trial jolts industry. . . . Merck had assembled the latest thinking on a 20-year quest . . . . had spent more than a decade devising the best ways . . . . the vaccine did not seem to be working. More people among the vaccinated group were getting the virus than those receiving a placebo. . . . roughly 90 percent of vaccine studies were using major elements of Merck’s approach. . . . John W. Shiver, who heads Merck’s basic research in vaccines . . . [and] is credited with several research advances, said he did not think any current approach would work. . . . a new burst of creativity was needed” [emphasis added].
—— Karl Stark, “Ending of HIV vaccine trial jolts industry Merck’s case was a failure of a product, not a failure of the vaccine’s concept”,, 7 October 2007.

2007: “[D]ata from . . . a 52 weeks clinical trial . . . did not show a clear advantage of . . . second generation HIV vaccine, IR103, over its original whole-killed HIV vaccine, REMUNE(R)”
—— “Orchestra Therapeutics discontinues its HIV vaccine development program”, PRNewswire-FirstCall, 17 July 2007;, accessed 18 July 2007 (broken link).

2007: “Scientists unveil piece of HIV protein that may be key to AIDS vaccine development”
—— NIH News, 14 February 2007; .

2007: “Novavax and collaborators significantly improve VLP vaccine for HIV/AIDS: Plans under way to advance new vaccine into clinical testing”
—— PRNewswire, 16 January 2007.

2008: “[T]he protein, FOX03a, shields against viral attacks and . . . the discovery will help in the development of a HIV vaccine”
—— “HIV breakthrough: Protein that fights immunodeficiency identified”,, 3 March 2008.

2008: “HIV isolate from Kenya provides clues for vaccine design”
—— EurekAlert, 2 January 2008
—— Blish et al., “Enhancing exposure of HIV-1 neutralization epitopes through mutations in gp41”, PLoS Med., 5 (#1, 2008) e9.

2008: Review: “Immune correlates of protection against HIV-1 infection”
—— Piacentini et al., “Not just sheer luck! Immune correlates of protection against HIV-1 infection”, Vaccine, 26 (2008) 3002-7.

2008: “Scientists are no further forward in developing a vaccine against HIV after more than 20 years of research, a Nobel Prize-winning biologist [David Baltimore] has said”
—— Helen Briggs, “HIV vaccine research hits impasse”, BBC News, 15 February 2008.

2008: “Despite hundreds and hundreds of millions of dollars, the reality in 2008 is that an HIV vaccine clearly remains beyond our grasp” [emphasis added]
—— Warner Greene, cochair of the HIV Vaccine Summit, cited in Bob Roehr, “NIH to Refocus HIV Vaccine Research”, 3April 2008;, accessed 10 April 2008 (broken link).

2008: “Critics fear worst for new SA HIV vaccine”
—— Bobby Jordan, Sunday Times (South Africa), 13 April 2008.

2008: Most scientists involved in Aids research believe that a vaccine against HIV is further away than ever and some have admitted that effective immunisation against the virus may never be possible, according to an unprecedented poll conducted by The Independent” [emphasis added]
—— Steve Connor & Chris Green, “Is it time to give up the search for an Aids vaccine? After 25 years and billions of pounds, leading scientists are now forced to ask this question”,, 24 April 2008; .

2012: “[N]ew and promising pathways …promising developments in HIV-1 vaccine design”
—— Kwong et al., “The changing face of HIV vaccine research”, J Int AIDS Soc., 15 (2012) 17407.

2013: “[A] major setback . . . volunteers who received the vaccination shot were more likely to contract the virus than those who were given a placebo. . . . Dr. Anthony Fauci called the results of the trial a ‘disappointment’ but added that the study yielded ‘important information’ that would help guide future research”
—— Katie McDonough, “Failed HIV vaccine clinical trial shut down — Researchers faced a major setback in the pursuit of an HIV vaccine after the shot was shown to be ineffective”,, 26 April 2013; .

*   *   *   *   *   *   *   *

With the Holy Grail and with unicorns, the intellectual mainstream of modern Western society has concluded that the anecdotal human testimony can be explained in other ways than the actual existence of the purported items. For various reasons, that conclusion has not yet been reached by a societal consensus on the matter of HIV vaccines. For one thing, HIV vaccines are taken to be matters of “science”, and society doesn’t disagree with whatever the mainstream consensus happens to be at any given time in any given scientific specialty. AIDS Rethinkers and HIV Skeptics, on the other hand, have very good explanations for the persistent failure of attempts to construct an HIV vaccine: HIV doesn’t exist.

How could I describe the evidence as “anecdotal and based on human testimony”? Simply because authentic virions of HIV have never been isolated direct from an “HIV-positive” individual. All research is based on so-called “isolates” of HIV, which are mixtures of many substances that originate in a particular density layer of solutions taken from cultures in which various active ingredients were mixed with material extracted from supposedly infected people. There is no gold-standard HIV test for this very reason; authentic naturally occurring HIV virions have never been demonstrated to exist. Yet vaccines are intended to work again such virions and their subsequent actions.

The mainstream HIV/AIDS literature is replete with the most intricate technical details and the most ingenious speculative attempts to explain results that should not be obtained if HIV/AIDS theory were correct. Yet every failure of HIV/AIDS theory just stimulates upholders of the faith to ever more arcane researches. One is reminded of the classic description of the sociology of cognitive dissonance: When the predicted Day of Judgment did not arrive on the calculated date, the underlying theory (=faith) was not questioned let alone abandoned; instead, new calculations delivered a new date — When Prophecy Fails: A Social and Psychological Study of A Modern Group that Predicted the Destruction of the World (Leon Festinger, Henry Riecken, & Stanley Schachter, Harper, 1956).

I acknowledged that my list of items is just a small sampling. PubMed is the abstracting and indexing service of the National Library of Medicine, National Center for Biotechnology Information, National Institutes of Health. A PubMed search for “HIV vaccine” yielded 15,000 results and for “AIDS vaccine” 10,000 results. There may be some duplication, but the number of technical articles published in the medical-scientific literature about vaccines against “HIV/AIDS” is at the very least 15,000 and may be in excess of 25,000; moreover, the vast majority of those will have described promising paths toward a vaccine, because disappointing results hardly ever get published.
Google Scholar returns 838,000 results for “HIV vaccine” and 510,000 for “AIDS vaccine”, indicating that interest beyond the strictly technical is high among academics, for example speculating about behavioral, economic, sociological aspects of a potential vaccine
The popular media amplify all these professional writings: A Google search for “HIV vaccine” yielded 20 million hits and 19 million for “AIDS vaccine”.

That’s a lot of words about something that may well be a mirage.

For lay people, the best way to think about the search for an HIV vaccine (or “AIDS vaccine”) is to recognize it as belonging to the genre of quests for the Holy Grail or for unicorns.

Posted in experts, HIV as stress, HIV does not cause AIDS, HIV skepticism, HIV transmission, uncritical media, vaccines | Tagged: | 31 Comments »

Youngest person sexually infected with HIV? How are pre-teens infected?

Posted by Henry Bauer on 2011/02/10

Teenaged boy contracted HIV through intercourse — A 13-year-old boy has become the youngest patient to contract HIV through sexual intercourse, health officials said. It is suspected the boy became infected while working part-time for a 50-year-old male, who used money to lure him into having sex, Centers for Disease Control (CDC) Deputy Director-General Lin Ting . . . said”.
This report is from China (Taiwan), but the same sort of nonsense could have come from anywhere.
The demographic characteristics of “HIV” — that is, of testing “HIV-positive” — make quite plain that “HIV” is not an infectious agent, let alone a sexually transmitted one. The evidence for that is set out in considerable detail in The Origin, Persistence and Failings of HIV/AIDS Theory, and more such evidence has been presented many times on this blog.
Consider the data from the Centers for Disease Control and Prevention from all public testing sites in the USA for the period 1995-98, as published in The Origin, Persistence and Failings of HIV/AIDS Theory [“F(HIV)” means the frequency of positive “HIV” tests, a term I used to avoid speaking about “HIV infection” or “HIV prevalence”]:

Now ask,

How did those people of various ages
become “HIV-positive”?
In particular, ages up to the teens?

At birth, babies carry antibodies generated by their mothers; 75% or more of “HIV-positive” babies got their “HIV” antibodies direct from their mothers, and lose them in less than a year; see  “Mother to child transmission of HIV and its prevention with AZT and Nevirapine — a critical  analysis  of  the  evidence” (2001) by the  Perth  Group, available at
By age 1, let alone ages between 1 and 12, babies and young children can therefore be “HIV-positive” only for some other reason than maternal antibodies. What could that reason be?
Note that the rate of “HIV-positive” continues to decline into the early teens. That was not owing to deaths reducing the number of “HIV-positives”, because in the 1990s no appreciable number of American babies or young children were dying of “HIV disease”.
Mother-to-child “transmission of HIV”, including via breast milk, had essentially ceased in the USA by the 1990s, so the only remaining means of infection would have been sexual transmission, dirty needles, or transfusion with contaminated blood. But, again, in the USA the two latter modes were almost unheard of by the mid-1990s, and sexual transmission (via sexual abuse, of course) is incredible at such high rates.
In any case, actual “infection” by any mechanism at all could not be the reason why these pre-teens tested “HIV-positive” since the rate of “HIV-positive” declined steadily, reaching a minimum in the low teens, and could not have been owing to deaths, as already remarked.
The only feasible explanation for the manner in which “HIV-positive” varies with age from birth into the teens is that testing  “HIV-positive” represents detection of substances that are associated with physiological stress, not an infectious agent. Birth is stressful, and children become physiologically stronger as their immune systems develop increasingly for years after birth. The Perth Group has published copious evidence that “HIV” tests are sensitive to and tend to test positive in the presence of oxidative stress.
That conclusion is underscored by the fact that the same variation of “HIV-positive” with age was found in healthy African subjects:

As a number of other posts on this blog have also illustrated, the manner in which “HIV-positive” varies with age is the same wherever and whenever such data are gathered, though the exact ages of the maxima and minima vary somewhat, in particular by race.

“HIV” tests do not detect a human immunodeficiency virus,
as consideration of the tests themselves already shows:
“HIV tests are not HIV tests”.

The mistaken belief that testing “HIV-positive” represents infection by a sexually transmitted agent has led to innumerable tragedies for some uncountable number of people: for instance, being needlessly fed toxic drugs, or being incarcerated for supposedly spreading a deadly infection, or becoming depressed upon being told that one is infected.

Posted in HIV as stress, HIV in children, HIV tests, HIV varies with age, sexual transmission | Tagged: | Leave a Comment »

Intestinal Dysbiosis theory confirmed

Posted by Henry Bauer on 2010/11/05

The thread on Questioning AIDS mentioned in the previous post is not only about oxidative stress and that HAART adds more such damage, it refers also to a number of articles that lend considerable support to Tony Lance’s hypothesis of intestinal dysbiosis:  damage to the intestinal microflora destroys safeguards — in particular against fungal infections — and allows leakage of certain substances from gut to blood which in turn leads to testing “HIV-positive”.
Mainstream work seems increasingly to be edging toward accepting this view. For example:
“the gastrointestinal tract plays a critical role in the pathogenesis of acute HIV-1 . . . infections”
— Mehandru et al., Journal of Allergy and Clinical Immunology, 116 (2005) 419-22.
“The gastrointestinal pathology associated with HIV infection comprises significant enteropathy with increased levels of inflammation and decreased levels of mucosal repair and regeneration”
— Brenchley & Douek, Mucosal Immunology, 1 (2008) 23-30
“Why and how HIV makes people sick is highly debated. Recent evidence implicates heightened immune activation due to breakdown of the gastrointestinal barrier as a determining factor of lentiviral pathogenesis. . . . Translocation of microbial products from the gut, in turn, correlates with increased immune activation in chronic HIV infection and may further damage the immune system . . . . Maintaining a healthy GALT [gut-associated lymphoid tissue] may be the key to reducing the pathogenic potential of HIV”
— Hofer & Speck, Seminars in Immunopathology, 31 (2009) 257-66.
“Reducing the pathogenic potential of HIV” by maintaining a healthy GALT is quite like Montagnier’s assertion, captured in the House of Numbers film,     that a healthy immune system can stave off damage from “HIV” (some discussion here). In practical terms — no theorizing about causes — these mainstream statements mean and recommend  precisely the same as Lance does:
You have more chance of staying healthy, whether you are “HIV-positive” or “HIV”-negative, if you don’t do anything to harm your beneficial gut microflora. Be sensible in terms of lifestyle. Pay special attention to diet, and by all means use probiotics.

*                    *                    *                    *                    *                    *                    *                    *

The mainstream has been unable to identify specific mechanisms by which “HIV” is supposed to kill off the immune system. The currently favored idea seems to be that “HIV” somehow brings about chronic systemic immune activation:
“the increased CD4+ and CD8+ cell death and proliferation is a consequence of virus-induced immune activation, not virus-mediated killing”
— Douek, PRN Notebook, 10(#3) (2005) 9-12.
“Chronic activation of the immune system is a hallmark of progressive HIV infection and better predicts disease outcome than plasma viral load” [emphasis added]
— Brenchley et al., Nature Medicine, 12 (2006) 1365-71
“HIV infection is characterized by chronic immune system activation” (review article)
— Nixon & Landay, Current Opinion in HIV and AIDS, 5 (2010) 498-503.

But how does “HIV” produce that condition?
“circulating microbial products, probably derived from the gastrointestinal tract, are a cause of HIV-related systemic immune activation. . . . These data establish a mechanism for chronic immune activation in the context of a compromised gastrointestinal mucosal surface”
— Brenchley et al., Nature Medicine, 12 (2006) 1365-71
“Microbial translocation has been linked to systemic immune activation during human immunodeficiency virus (HIV) type 1 infection. Here, we show that an elevated level of microbial translocation . . . correlates with AIDS”
— Nowroozalizadeh et al., Journal of Infectious Diseases, 201 (2010) 1150-4.
So, again, precisely the Lance hypothesis: Damage to the gut’s protective functioning allows leakage into the blood of substances not normally there, producing chronic activation so long as the leakage persists. Eventually serious illness can result.

The salient difference between the Lance theory and the mainstream belief is this:
— If Lance is right, then damage to the gut microflora precedes whatever markers may be used to detect what is thought to be “HIV” or to diagnose what is considered “AIDS”.
— If the mainstream view is correct, then “HIV infection” causes the damage to the gut.

Now, according to Sankaran et al., Journal of Virology, 82 (2008) 538-45:
“HIV-induced pathogenesis in GALT [gut-associated lymphoid tissue] emerges at both the molecular and cellular levels prior to seroconversion in primary HIV infection, potentially setting the stage for disease progression by impairing the ability to control viral replication and repair and regenerate intestinal mucosal tissues. . . . deterioration of the intestinal mucosa may initiate rapidly following infection . . . . HIV-induced enteropathy is well established within the first few weeks of infection, potentially even prior to seroconversion” [emphases added].
The examined biopsy samples had been obtained “at 4 to 8 weeks following HIV infection”; 3 of the 4 patients were then HIV-negative, and the 4th seroconverted 2 days before the biopsy. “Four highly active antiretroviral therapy (HAART)-naive patients in the primary stage of HIV infection (4 to 8 weeks postinfection)” were studied. However, it is not explained how these individuals happened to be enrolled in this study and to be under observation even before seroconversion. The only mentioned reason for assuming “HIV infection” were “flu-like” symptoms, and at that time they tested HIV-negative. Cited earlier studies by the same authors give no more specific information about these individuals; the only clue is that the work seems to be associated with the Center for AIDS Research, Education and Services in Sacramento (CA): so perhaps gay men enroll who are concerned that they might be exposed to “HIV” and might at some time seroconvert?
At any rate, it seems permissible to doubt that the date of “HIV infection” could have been accurately known. But in any case this is immaterial for the present purpose. What is clear is that at some time prior to testing “HIV-positive”, these four individuals had experienced damage to the mucosal lymphoid tissue of the sort seen in “HIV disease” or “AIDS”.
That is precisely what Lance’s intestinal dysbiosis theory predicts.
The mainstream belief is that “HIV infection” immediately — albeit it not always! — produces “flu-like” symptoms, but that antibodies do not appear for several weeks. It seems at least equally plausible that damage to the gut’s immune system brings gut leakage and immune activation that immediately causes “flu-like” symptoms. After all, those symptoms — fever in particular — are the direct result of activation of the immune system as it responds to foreign presences.

*                    *                    *                    *                    *                    *                    *                    *

When Tony had first told me of his theory, it came as the answer to what had been for me the most puzzling aspect of the HIV/AIDS story, from the viewpoint of one who had already seen that “HIV” is not what it’s said to be. The puzzle was, why gay men tested “HIV-positive” at such high rates; even though many of them remained seemingly healthy; and why testing positive seemed maximally probable at ages in the thirties or early forties. The intestinal dysbiosis theory explains those: A certain degree of dysbiosis can produce a positive “HIV” test without causing significant ill health; but continuing damage to the gut microflora over a decade or two could bring ill health as well as testing “HIV” positive.

At the Oakland Conference, Tony described how he came to his theory. The abstract, slides, audio, and video of his talk are available at the Conference website.
(The YouTube version of Part 2 seems  to stop before the end of Tony’s talk.)
Watching that video, one must surely be impressed by the strength of character this man has displayed. He disclaims expertise in science, but Tony Lance has demonstrated the single most important feature of doing science properly: an unwavering determination to look at all the evidence and then to seek explanations for it.

Posted in clinical trials, HIV as stress, HIV does not cause AIDS, HIV risk groups, HIV skepticism, HIV tests | Tagged: , | 32 Comments »

HAART makes things worse: Elsevier journal publishes HIV/AIDS heresies

Posted by Henry Bauer on 2010/11/03

Tony Lance alerted me to a discussion on Questioning AIDS started by trueverax with links to some fascinating recent articles about “HIV” and oxidative stress, for example, Gil et al., “Altered oxidative stress indexes related to disease progression marker in human immunodeficiency virus infected patients with antiretroviral therapy”, Biomedicine & Pharmacotherapy (2010), doi:10.1016/j.biopha.2010.09.009; the journal is published by Elsevier Masson France.
This in-press article in an Elsevier journal seems no less heretical than those Elsevier withdrew a year ago from Medical Hypotheses after protests from HIV/AIDS vigilantes. As Tony had remarked, “The opening line probably caused the Perth Group to chuckle — or sob”. Indeed:

“It is generally accepted that oxidative stress (OS) is implicated
in immunological and metabolic abnormalities during HIV infection”

Beginning in the 1980s, the Perth Group has argued:
“That AIDS and all the phenomena inferred as ‘HIV’ are induced by changes in cellular redox brought about by the oxidative nature of substances and exposures common to all the AIDS risk groups and to the cells used in the ‘culture’ and ‘isolation’ of ‘HIV’”.
For example,
“There is no compelling reason for preferring the viral hypothesis of AIDS to one based on the activity of oxidising agents” — Eleni Papadopulos-Eleopulos, “Reappraisal of AIDS: Is the oxidation induced by the risk factors the primary cause?”, Medical Hypotheses 25 (1988)151-162.

The remarkable statement in the Abstract of Gil et al’s article, that the presence of oxidative stress in “HIV/AIDS” is “generally accepted”, is repeated in the text in this way:
“The redox balance is also severely disturbed in HIV infected individuals without HAART [7–13].” Those references are:
[7] Israel et al., Cellular and Molecular Life Sciences, 53 (1997) 864-70.
[8] Romero-Avila et al., Medical Hypotheses, 51 (1998) 169-73.
[9] Sönnerborg et al., Scandinavian Journal of Infectious Diseases, 20 (1988) 287-90.
[10] Favier et al., Chemico-biological Interactions, 91 (1994) 165-80.
[11] Allard et al., American Journal of Clinical Nutrition, 67 (1998) 143-7.
[12] Gil et al., Pharmacological Research, 47 (2003) 217-24.
[13] Pasupathi et al., Journal of Scientific Research, 1 (2009) 370-80.

I noticed that these seven articles, as well as the one in Biomedicine & Pharmacotherapy, are all in journals that do not specialize in HIV/AIDS. Yet the substance of these articles concerns HIV/AIDS more directly than it does anything else. Here’s a little research project for someone who has some time: Ask the authors of these articles whether they had tried to publish in a journal like JAIDS; and if not, why not?

Here’s another interesting fact about these articles: All the work was done outside the United States. Gil et al. worked in Cuba; Israel et al. in France; Romero-Alvira in Spain; Sönnerborg et al. in Sweden; Favier et al. in France; Allard et al. in Canada; Gil et al., 2003, in Cuba but with a co-worker in Italy; Pasupathi et al. in India.
It may not seem surprising, therefore, that none of these articles acknowledge research support from an American source. That is, it may not seem surprising to people not familiar with the fact that the National Institutes of Health (as well as a number of American foundations) do support considerable amounts of research outside the United States. Perhaps especially about HIV/AIDS; much research on HIV/AIDS in Africa, for example, is supported by American money.
But then again, it’s certainly no surprise that the National Institutes of Health would not support research on the role of oxidative stress in the conditions that are labeled “HIV-positive” or “AIDS”.

The discussion on Questioning AIDS also cites another study, from Africa, that reports correlation of “HIV-positive” status with lowered antioxidant activity: Bilbis et al., Annals of African Medicine, 9(#4) (2010) 235-9; not an AIDS-specialist journal, no research support acknowledged.

Now Gil et al. do not state outright that oxidative stress might be the cause of “HIV-positive” or of “AIDS”, they only point out that oxidative stress is present in those conditions. However, given that “HIV” virions have never been isolated from “HIV-positive” individuals, it is no great step from these findings to the stance taken by the Perth Group for more than two decades.
None of these articles cite the Perth work, of course. Even Romero-Alvira, who published in Medical Hypotheses in 1998, does not cite the 1988 Papadopulos-Eleopulos article in Medical Hypotheses.

*                    *                    *                    *                    *                    *                    *                    *

But the greatest heresy of Gil et al. (2010) lies not in pointing out the role of oxidative stress in HIV/AIDS: It is the finding, in a placebo-controlled trial, that HAART makes things worse.
A variety of measures of oxidative stress were used. Three groups of “HIV-positive” individuals were studied: One not subjected to antiretroviral drugs; one treated with AZT/3TC/ IND (zidovudine or Retrovir, a NRTI; lamivudine, a NRTI; indinavir, a protease inhibitor); one treated with D4T/3TC/ NEV (stavudine, Zerit, a NRTI; lamivudine, a NRTI; nevirapine or Viramune, a NNRTI):
“both combination . . . produced an increase in OS [oxidative stress] indexes paralleled to HIV progression marker change”; in the second (D4T) group to the extent that there was “a poor prognostic” under this treatment.
References are cited for the toxicity of HAART, including typical damage to mitochondrial function. The mitochondria are the energy-producing sites of all animal cells and play a significant role in the redox systems within all cells.
Perhaps most significant, it is pointed out that the surrogate markers typically used to assess the success of HAART, CD4 counts and viral load, did show “improvement” under HAART in these studies at the same time as oxidative stress increased:

increasing OS . . . occurs . . .
during apparently successful  HAART.
This  . . .  underline[s] HAART associated toxicity

[emphasis added].

This work serves to explain quite a few things about “HIV/AIDS” and HAART, for example that neither CD4 counts nor viral load is a good predictor of clinical outcomes (Rodriguez et al., JAMA, 296 (2006) 1498-1506).

Another reference cited in this thread on Questioning AIDS confirms the finding of increased oxidative stress as a result of HAART:

“HAART may affect oxidative stress in HIV-1-infected patients
. . . antiretroviral therapy plays an important role
in the synergy of HIV infection and oxidative stress”

(PMID: 19884983, Mandas et al., Journal of Biomedicine & Biotechnology, 2009;2009:749575. Epub 2009 Oct 26 — again, not an AIDS-specialist journal; work done in Italy).

Posted in antiretroviral drugs, clinical trials, experts, HIV as stress, HIV does not cause AIDS, HIV skepticism | Tagged: | 4 Comments »