HIV/AIDS Skepticism

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

Posts Tagged ‘intestinal dysbiosis’


Posted by Henry Bauer on 2009/09/28

“A nutritional formula . . . may help slow CD4 cell decline and reduce immune activation” [Liz Highleyman, reporting on  “Reduced CD4+ T cell decline and immune activation by NR100157, a specific multi-targeted nutritional intervention, in HIV-1 positive adults not on antiretroviral therapy (BITE)” by J. Lange et al., presented at the 49th Interscience Conference on Antimicrobial Agents and Chemotherapy, San Francisco, 12-15 September 2009; Abstract H-1230b].
“Pedro Cahn and colleagues with the international BITE study aimed to determine whether a combination nutritional formula could reduce CD4 cells loss in people on ART. The randomized controlled trial was designed to include 800 HIV positive participants in Argentina, Australia, Brazil, Italy, the Netherlands, Thailand, the U.K., and the U.S. Half were randomly assigned to take the nutritional formula, known as NR100157, for 1 year, while the other half received a control product containing the same amount of calories and protein, but without the active ingredients. NR100157 contains several components that individually have demonstrated beneficial effects on immune function in previous studies: Prebiotic oligosaccharides: chains of simple sugars that help maintain healthy flora, or balance of bacteria in the gut; N-acetyl cysteine: a modified amino acid that helps maintain the body’s supply of glutathione, a key antioxidant; Bovine colostrum: nutrient- and antibody-rich fluid produced prior to milk; Omega-3 long-chain polyunsaturated fatty acids: molecules shown to improve the integrity of the gut, which prevents bacteria from leaking out and triggering systemic immune activation; Micronutrients including vitamins and minerals.
The study was stopped early after a planned interim analysis showed significant immunological benefit in the NR100157 arm and no notable safety concerns. . . .
Participants in the NR100157 arm lost significantly fewer CD4 cells per year than those in the control arm (-28 vs -68 cells/mm3, respectively; expected loss for untreated people with HIV 50-70 cells/mm3 annually). There were no significant differences between the 2 arms with regard to CD4 percentage, CD8 cell count, or CD4/CD8 ratio. Plasma viral load remained stable, and similar, in both groups” [emphases added].

1. Maintaining healthy gut flora benefits immune function: that’s what Tony Lance discussed in his intestinal dysbiosis hypothesis, including the aspect of gut leakage, systemic immune activation, and potentially testing “HIV-positive” [“What really caused AIDS: Slicing through the Gordian Knot”, 20 February 2008].

2. The “viral load” was stable while CD4 counts varied: in other words, once again, changes in CD4 counts do not correlate with “viral load” [Rodriguez et al., JAMA, 296 (2006) 1498-1506].

3. HIV/AIDS mainstreamers are much more critical of clinical trials of alternative remedies than they are of mainstream endeavors. When mainstreamers publish at “statistical significance” of p<0.05 — wrong once in 20 times —, that’s good; but when an alternative treatment is significant at p=0.03 —  wrong only once in 33 times — that’s cause for HAART enthusiasts and HIV/AIDS believers to be “stunned” that anyone would accept it (“Gut-shielding mix slows CD4 drop in people not taking antiretrovirals”) :
“The data and safety monitoring board (DSMB) recommended stopping BITE early because of a significant difference in CD4 decline between groups and lack of safety concerns. An intention-to-treat analysis at 52 weeks showed a significantly slower annual average CD4-cell drop in the NR100157 group, 28 versus 68 cells/mm(3) with placebo (P = 0.030). . . . In a question-and-answer session after Argentina’s Pedro Cahn presented these findings, Harvard’s Daniel Kuritzkes claimed to be ‘stunned’ that the DSMB would stop the trial of an apparently safe agent when the statistical difference between treatment arms reached only 0.03. He also questioned the investigators’ decision to take the DSMB’s advice. Kuritzkes felt stopping a trial at such a low level of significance leaves open the possibility of bias toward a positive finding” [emphases added].
I suppose Kuritzkes would have been even more astonished that researchers stopped trials of circumcision early on the basis of the usual “95% confidence interval” — i.e., wrong once in 20 times; or that they were ecstatic over the first apparent success of a vaccine trial after many failures, even though one would have expected such an APPARENT success sooner or later at that usual “p<0.05”, “wrong once every 20 times”, criterion.

To be quite clear:
I agree that a single clinical trial is inconclusive, no matter what level of statistical significance may be reached.
I agree that p=0.03 is not in itself a particularly convincing result; still less so, of course, are all the mainstream trials that accept the weaker p<0.05; not to speak of the statistical ignorance that allows researchers at the Centers for Disease Control and Prevention  and elsewhere to confuse correlation with causation and to say such things as “nonsignificantly lower” [“Abuses of statistics in HIV/AIDS research”, 14 September 2009].
My point here is just that alternative treatments are criticized while even worse examples of mainstream contentions are given free passes or even praised.

Posted in Alternative AIDS treatments, clinical trials, HIV as stress, HIV does not cause AIDS, HIV skepticism | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , | 4 Comments »

“HIV” and illness: Which comes first?

Posted by Henry Bauer on 2009/07/23

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.

Posted in Alternative AIDS treatments, HIV as stress, HIV does not cause AIDS, HIV risk groups, HIV skepticism, HIV tests | Tagged: , , , , , , , , | 10 Comments »

HAART saves lives — but doesn’t prolong them!?

Posted by Henry Bauer on 2008/09/17

Death rates are down, yet AIDS patients are not living longer! Why not?

(This is a long post, and includes at least one Table that is too large to be viewed conveniently in the same window as the text. If you prefer to read it as a pdf, here it is: haartdoesnt-prolong-lives)

In the early 1980s, a diagnosis of “AIDS” typically had been followed by death within a year or two. At that time, diagnosis was on the basis of Kaposi’s sarcoma or of manifest opportunistic fungal infections — Pneumocystis carinii pneumonia or candidiasis.

Following the adoption of “HIV-positive” as a necessary criterion for an AIDS diagnosis, an increasing range of non-opportunistic infections and other illnesses came to be included as “AIDS-defining” (for instance, tuberculosis, wasting, cervical cancer, etc.) — see Table 1; the most consequential changes were in 1987 and in 1993. The only basis for them was that people with some illnesses were quite often “HIV-positive”, in other words, there were correlations with “HIV-positive” status, not any proof that “HIV encephalopathy”, “HIV wasting disease”, or other additions to the list of “AIDS-defining” conditions were caused by “HIV”. Indeed, there could not be such proof since mechanisms by which “HIV” could cause illness have not been demonstrated, and they remain to this day a matter for speculation — even over the central issue of how HIV (supposedly) kills immune-system cells. An absurd consequence of these re-definitions, often cited by HIV/AIDS skeptics, is that a person suffering indisputably from tuberculosis (say) might or might not be classed as an HIV/AIDS patient, depending solely on “HIV” tests.

Table 1

(from Nakashima & Fleming, JAIDS 32 [2003] 68-85; numbers in parentheses after the dates refer to sources cited in that article)

As “AIDS” was being diagnosed increasingly among people less desperately ill than the original AIDS victims, survival time after diagnosis became longer.

The 1993 change extended the umbrella of “AIDS patient” to cover people with no manifest symptoms of ill health; in ordinary parlance, they weren’t ill, and consequently the interval between an AIDS diagnosis and death was bound to increase dramatically. This re-definition also expanded enormously the number of “AIDS cases”: about 70% of them are not ill (Walensky et al., Journal of Infectious Diseases 194 [2006] 11-19, at p. 16).

In 1996, earlier treatment for AIDS with high-dose reverse transcriptase inhibitors like AZT (ZDV, Retrovir) was increasingly superseded by “highly active antiretroviral treatment” (HAART), which has been generally credited with the prolonging of lives by a considerable number of years. According to the Antiretroviral Therapy Collaboration (Lancet 372 [2008] 293-99), life expectancy for 20-year-old HIV-positives had increased by 13 years between 1996 and 2005 to an additional 49 years; for 35-year-olds, the life expectancy in 1996-99 was said to be another 25 years. According to Walensky et al. (op. cit.), survival after an AIDS diagnosis now averages more than 14 years. Yet another encomium to antiretroviral drugs claims that “by 2004-2006, the risk of death in the first 5 years following seroconversion was similar to that of the general population” (Bhaskaran et al., JAMA 300 [2008] 51-59).

There is general agreement, then, that antiretroviral treatment has yielded substantial extension of life to people already diagnosed with AIDS. The interval between an AIDS diagnosis and death should now be measured in decades rather than a year or two.

As with so many other contentions of orthodox HIV/AIDS belief, however, this expectation is contrary to actual fact. The greatest risk of death from “HIV disease” comes at ages in the range of 35-45, just as at the beginning of the AIDS era. There was no dramatic increase in median age of death after 1996 following the adoption of HAART, see Table 2:

Table 2
Age Distributions of AIDS Diagnoses and AIDS Deaths, 1982-2004
from annual “Health, United States” reports

The slow, steady increase in median ages of AIDS diagnosis and of death shown in Table 2 is pictured in Figure 1, below. The slope of the curve for median age of death shows no pronounced turn upwards following 1996 — even though the annual numbers of deaths decreased by more than half between 1994 and 1998. The somewhat steeper increase in median age of death from 1997 to 1999 and the parallel sharper increase in median age of AIDS diagnosis are both artefacts stemming from re-calculation of numbers under a revised International Diagnostic Code, see asterisked footnote to Table 2. The other slight discontinuity in the curve, around 1993, reflects the CDC’s revised definition of AIDS to include asymptomatic HIV-positive people with low CD4 counts.

Figure 1

The uppermost curve, the interval between median age of diagnosis and median age of death underscores that over the whole course of the AIDS era, no episode brought a significant increase in median age of death, other than the drastic expansion of definition in 1992-93. (Of course, the difference between the median ages for diagnosis and death in any given year cannot be equated with the interval between diagnosis and death for any given individual; the significant point in Figure 1 is just that median ages have changed at a gradual and almost constant rate from the very beginning of the AIDS era. HAART changed the death rate dramatically, but not the ages at which people died.)

This constitutes a major conundrum, a paradox: If HAART has extended life-spans by the claimed amounts, then why has not the median age of death increased dramatically? Why were so many AIDS patients still dying around age 45 in 2004?

The resolution of this conundrum is that the median ages of death are based on actually recorded deaths, whereas the claimed benefits of HAART were calculated on the basis of models incorporating many assumptions about the course of “HIV disease” and relying on contemporaneous death-rates [Science Studies 103: Science, Truth, Public Policy — What the CDC should know but doesn’t, 4 September 2008; CDC’s “model” assumptions (Science Studies 103a), 6 September 2008].

The numbers for total AIDS cases and for deaths, shown graphically in Figure 1, are listed in Table 3. There, column III shows the numbers of survivors in any given year, calculated from the difference between cases and deaths in earlier years plus new cases in the given year. Column IV has the percentage of survivors who died each year.

Table 3
Total AIDS cases, deaths, and
survivors “living with HIV/AIDS”,

From 1996 to 1997, the annual numbers of deaths halved, and of course the percentage of deaths among survivors also halved. Since 1997, only between 2.8 and 5.7% of living “HIV/AIDS” patients have been dying annually, which is in keeping with the claims of life-saving benefits made for HAART on the basis of death rates and computer models. But that conflicts with the age distribution of deaths, which has remained without major change during those same years.

If AIDS patients are now enjoying a virtually normal life-span, who are the people still dying at median age 45? If HAART is saving lives, why aren’t those lives longer?

The reason is that testing “HIV-positive” is actually irrelevant to the cause of death. It does not indicate infection by a cause of illness, it is an indicator analogous to fever. Many conditions may stimulate a positive “HIV” test: vaccination against flu or tetanus, for example; or tuberculosis; or drug abuse; or pregnancy; and many more (Christine Johnson, “Whose antibodies are they anyway? Factors known to cause false positive HIV antibody test results”, Continuum 4 (#3, Sept./Oct. 1996).

The likelihood that any given individual exposed to one of those conditions will actually test positive seems to correlate with the seriousness of the challenge to health; and it varies in a predictable manner with age, sex, and race (The Origin, Persistence and Failings of HIV/AIDS Theory). In any group of people, those who test “HIV-positive” are more likely to be or to become ill, so they are also more likely to die than those who do not test positive: just as in any group of people, those who have a fever are more likely to be ill and to die than those who do not have a fever. Also, of course, a fever does not necessarily presage death, nor does “HIV-positive” necessarily presage death; and in any group of people, some will die who never tested positive or who never had a fever. There’s a strong correlation between illness, death, and fever, but it’s not an inevitable one and fever is not the causative agent; there’s a strong correlation between illness, death, and “HIV-positive”, but it’s not an inevitable one and “HIV” is not the causative agent.

So: Among people “living with HIV/AIDS”, those who happen to die in any given year are simply ones whose “HIV-positive” status was associated with some actually life-threatening illness; and their ages were distributed just as ages are distributed in any group of “HIV-positive” people, with a median age at around 40, with minor variations depending on race and sex. For example, in 2000, there were more than 350,000 people “living with HIV/AIDS” (Table 3) whose median age was somewhere around 39.9 (Table 2: 39.9 was the median age of new diagnoses in that year. Survivors from the previous year , when the median age had been 39.4, would have had a median age — one year later — somewhere between 39.4 and 40.4; not as much as 40.4, because those dying in 1999 had a higher median age than those who didn’t die.) Of the 350,000 in 2000 with median age 39.9, 3.9% (14,457, Table 3) died; and the median age of those dying was 42.7. It’s only to be expected, of course, that — among any group of people at all — those who die have a somewhat higher average age than those who don’t die in that year.

The rate of death among “HIV/AIDS” patients declined markedly from 1987 to 1992 simply because “HIV/AIDS” was being increasingly defined to include illnesses less life-threatening than the original AIDS diseases of Kaposi’s sarcoma and established opportunistic fungal infections. Another sharp drop in death rates came after 1992 when people who were not even ill came to be classed as “HIV/AIDS” patients and comprised about 70% of such patients. The last sudden drop in death rates, with the introduction of HAART in 1996, resulted not from any lifesaving benefit of HAART but because the latter superseded the earlier, much more toxic, high-dose regimens of AZT. The supposed benefits of HAART are to decrease viral load and allow CD4 counts to rise; but these effects come slowly and cannot explain a sudden improvement in clinical condition sufficient to bring a halving of deaths from one year to the next; on the other hand, stopping the administration of a highly toxic substance can certainly bring numbers of deaths down immediately. These data indicate, therefore, that something like half (at least) of “HIV/AIDS” deaths from 1987 through 1996 — some 150,000 — are attributable to the toxicity of AZT.

Through all those drastic as well as slower changes in death rates, among those “HIV/AIDS patients” who died for any one of a large variety of reasons, the median age of the “HIV-positive” ones remained about the same as it had always been. “HIV/AIDS” patients are not living longer despite the change in death rate from an annual 60% or more to 3% or less.

As I said in a previous post [How “AIDS Deaths” and “HIV Infections” Vary with Age — and WHY, 15 September 2008], this paradox follows “from the manner in which HIV tests were designed and from the fact that AIDS was defined in terms of ‘HIV’”. The genesis of the tests has been described lucidly by Neville Hodgkinson (“HIV diagnosis: a ludicrous case of circular reasoning”, The Business, 16/17 May 2004, pp 1 and 4; similar in “The circular reasoning scandal of HIV testing”, thebusinessonline, 21 May 2006):

“It never proved possible to validate the [HIV] tests by culturing, purifying and analysing particles of the purported virus from patients who test positive, then demonstrating that these are not present in patients who test negative. This was despite heroic efforts to make the virus reveal itself in patients with Aids [sic, British usage] or at risk of Aids, in which their immune cells were stimulated for weeks in laboratory cultures using a variety of agents.
After the cells had been activated in this way, HIV pioneers found some 30 proteins in filtered material that gathered at a density characteristic of retroviruses. They attributed some of these to various parts of the virus. But they never demonstrated that these so-called ‘HIV antigens’ belonged to a new retrovirus.
So, out of the 30 proteins, how did they select the ones to be defined as being from HIV? The answer is shocking, and goes to the root of what is probably the biggest scandal in medical history. They selected those that were most reactive with antibodies in blood samples from Aids patients and those at risk of Aids.
This means that ‘HIV’ antigens are defined as such not on the basis of being shown to belong to HIV, but on the basis that they react with antibodies in Aids patients. Aids patients are then diagnosed as being infected with HIV on the basis that they have antibodies which react with those same antigens. The reasoning is circular.”

“HIV” tests were created to react most strongly to substances present in the sera of very ill gay men whose average age was in the late 30s (Michelle Cochrane, When AIDS began: San Francisco and the making of an epidemic, Routledge, 2004; cited at pp. 188-92 in The Origin, Persistence and Failings of HIV/AIDS Theory). That’s why people who are in some manner health-challenged are more likely than others to test “HIV-positive”, especially if they are aged around 40. Evidently the particular molecular species picked up by “HIV” tests are generated most prolifically around age 40, especially under the stimulation of various forms and degrees of physiological stress. That’s why the median ages for testing “HIV-positive” and for being diagnosed with AIDS (criterion: positive HIV test) and for dying from HIV/AIDS  (criterion: positive HIV test) are all the same, in the range 35-45.

Perhaps some of what “HIV” tests detect are so-called “stress” or “heat-shock” proteins. That gay men so often test “HIV-positive” might have to do with molecular species associated with “leaky gut syndrome” or other consequences of intestinal dysbiosis [What really caused AIDS: slicing through the Gordian knot, 20 February 2008].

Those are speculations, of course. What is not speculative, however, is that HAART does not prolong life* even as it lowers death rates. It is also clear that testing “HIV-positive” is no more than an indicator of some form of physiological challenge, not necessarily infection by a pathogen and specifically not infection by a retrovirus that destroys the human immune system.

Even as it is obvious that HAART does not prolong life on the average, there are reliable testimonies that individuals have experienced clinical improvement on HAART, often dramatic and immediate. But, again, such immediate benefit cannot be the result of antiretroviral action, and likely reflects an antibiotic or anti-inflammatory effect, as suggested by Dr. Juliane Sacher [Alternative treatments for AIDS, 25 February 2008].

Posted in antiretroviral drugs, HIV and race, HIV as stress, HIV does not cause AIDS, HIV tests, HIV varies with age, HIV/AIDS numbers | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , | 5 Comments »


Posted by Henry Bauer on 2008/05/23

According to HIV/AIDS dogma, testing “HIV-positive” denotes infection by “HIV” which is permanent and ineradicable. One of several independent proofs that HIV/AIDS theory is wrong is the fact that people do spontaneously revert from “HIV-positive” to “HIV”-negative, perhaps most notably and frequently, babies born “HIV-positive” and reformed drug abusers (p. 96 ff. in The Origin, Persistence and Failings of HIV/AIDS Theory). But whenever spontaneous reversion happens to be noticed, it’s treated as the secular equivalent of a miracle (HIV “INFECTION” DISAPPEARS SPONTANEOUSLY, 22 January 2008). Here are a couple more instances:

BEIJING, Dec. 3 (Xinhua) — A farmer in northeast China’s Jilin Province has tested HIV negative, six years after being diagnosed as HIV-positive, according to the provincial Center of Disease Control (CDC).
Wen Congcheng . . . first tested HIV positive in 2001 [during testing of blood donors]. . . . Late in 2003, he was re-confirmed to have HIV/AIDS as a result of another test . . . . However, in July this year [2007], Wen received a negative test result at the No. 1 Clinical Hospital of Beihua University in Jilin. Wen decided to seek another opinion and went to the First Hospital of the China Medical University and another three hospitals for HIV tests, which all proved to be negative. The Jilin municipal CDC carried out a follow-up test which confirmed the negative result, and later the provincial CDC also confirmed the result.”

But, of course, the white-coated gurus refuse to accept this, and have questioned the original positive result, while the lab that made the diagnosis sticks by it.

“ ‘I am pretty sure there are no problems with the blood samples and the tests,’ said Liu Baogui, former director of the HIV/AIDS and STD Section of the CDC of Jilin City. . . . Professor Wu Min, a member of the HIV/AIDS experts’ committee under the Ministry of Health, is sceptical about the validity of the original positive test result. ‘I can not believe that such miracle could have really happened,’ he said. ‘Some patients appear to be free of the virus after effective treatment, but the HIV anti-body is always there, so the test result will still be positive.’ Wu said the inaccuracy rate of tests by the provincial CDCs is lower than 0.01 percent. ‘But it is possible that the person’s name and blood sample was mixed up at the Chuanying District CDC where Wen tested HIV positive for the first time,’ he said.
. . .
In 2003, Andrew Stimpson, a 25-year-old Briton, tested HIV-negative 14 months after testing positive in May 2002. The case has never been scientifically explained.”

And here’s more detail about Andrew Stimpson:

“Doctors baffled as HIV man ‘cures’ himself” (Sophie Kirkham, Sunday Times, 13 November 2005)

“A MAN who tested positive for HIV, the virus that causes Aids [sic, British usage], has subsequently shown up negative for the disease in a case that has mystified doctors. It was claimed last night that Andrew Stimpson, 25, may have shaken off the virus with his own immune system after contracting HIV in 2002.
If proved, the NHS has said the case would be ‘medically remarkable’. … The Chelsea and Westminster Healthcare NHS trust, which treated Stimpson, has said he needs to undergo more tests before it can be established how he apparently conquered HIV. ‘These tests were accurate and they were his, but what we don’t know at the moment is why that has happened, and we want him to come back in for more tests… It is potentially a fantastic thing.’ Stimpson was tested three times in August 2002 … and the results showed he was producing HIV antibodies to fight the disease. Stimpson … contracted the virus from his boyfriend, Juan Gomez, 44. He began taking vitamins and other dietary supplements to keep his body healthy in the hopes that this might fend off the development of full-blown Aids. In October 2003, after impressing doctors with his good health, Stimpson was offered a new test, which came back negative. Further tests in December 2003 and March last year also proved negative. … ‘I couldn’t understand how anyone could cure themselves of HIV . . . I thought it had to be wrong because no one can recover from HIV, it just doesn’t happen.’ The tests were re-checked by the Chelsea and Westminster Healthcare NHS Trust when Stimpson threatened litigation believing there must be a mistake, but the results confirmed all the tests had been accurate. In a letter understood to be from the NHS Litigation Authority in October this year, Stimpson was told: ‘The fact you have recovered from a positive antibody result to a negative result is exceptional and medically remarkable.’ The trust said there had been several other cases of claimed ‘spontaneous clearance’ of the virus worldwide, although it is not believed any have been proved. A spokeswoman added that the trust had urged Stimpson to return for tests, but that so far he had not done so.”

If I were Stimpson, I too would decline further tests administered by people who would love to be able to tell me that I do, after all, have an incurable and fatal illness. Stimpson’s case is readily explicable by Tony Lance’s intestinal dysbiosis hypothesis [WHAT REALLY CAUSED AIDS: SLICING THROUGH THE GORDIAN KNOT, 20 February 2008] or by the Perth-Group view that testing HIV-positive merely denotes oxidative stress. It was not that Stimpson “contracted the virus from his boyfriend”, but that they shared a lifestyle conducive in some manner to oxidative stress or intestinal dysbiosis.

Posted in experts, HIV as stress, HIV does not cause AIDS, HIV skepticism, HIV tests, HIV transmission, sexual transmission | Tagged: , , , , , , , | 7 Comments »


Posted by Henry Bauer on 2008/03/08

I had described Tony Lance’s article on intestinal dysbiosis as “slicing through the Gordian knot” [20 February 2008] because it offers coherent and plausible answers to the most vexing specific mysteries about “AIDS”. It appeared around 1980 among gay men in a few large cities: Why then? Why there? Why in the form of those particular diseases—KS, PCP, candidiasis? In addition, Lance’s explanation offers a satisfactory resolution to what has been a salient conundrum for HIV/AIDS dissidents: Why does antiretroviral treatment sometimes bring tangible, almost immediate health benefits?

Some of the responses to Tony’s article have brought home to me the need to put this keystone solution into perspective, because “HIV/AIDS” nowadays encompasses such an enormous range of disparate things. It’s an exceedingly complicated mess, with many threads needing to be unraveled even after the central knot has been sliced.

To begin with, one must recognize that

1. “HIV” and “AIDS” are distinctly separate things.
2. Neither “HIV” nor “AIDS” is definitively defined by universally agreed, substantive and objective criteria.
3. That second point is illustrated by the way in which the definitions of “HIV” and of “AIDS” have been changed or augmented over time.
4. To muddy the waters even further, in some circumstances—but not in others—there is an indirect correlation between some claimed measures of “HIV” and the claimed incidence of some forms of “AIDS”.


1. “HIV” and “AIDS” are two separate things

Chapter 9 in The Origin, Persistence and Failings of HIV/AIDS Theory summarizes the many facts which show that “HIV” and “AIDS” are not correlated:
— “HIV”-negative AIDS cases
— “HIV”-positive people who never come down with an “AIDS-defining” illness
— male-to-female ratios for “AIDS” and for “HIV” are quite different; and the difference has changed over the years
— black-to-white ratios for “AIDS” and for “HIV” are quite different; and the difference has changed over the years
— the overall incidence and prevalence of “AIDS” and of “HIV” have changed quite differently over the years
— the geographic distributions of “AIDS” and of “HIV” are not the same

2 & 3. “HIV” and “AIDS” have not been defined definitively; definitions have changed over time

“AIDS”, when first recognized as a distinct entity, was defined as an immunedeficiency marked by rare opportunistic infections and having no obvious cause (i.e., no cancer, malnutrition, or other condition known to suppress immune function).
After the claimed discovery of “HIV” as its cause, “AIDS” was re-defined to require a positive “HIV”-test. That made it necessary, some years later, to invent the new phenomenon of idiopathic CD4-T-cell lymphopenia—pathogenic immunedeficiency without obvious cause—to describe cases where the clinical diagnosis would have been “AIDS” except that “HIV”-tests were negative.
The inclusion of hemophiliacs under “AIDS” broke the initial definition of immunedeficiency for no known reason.
Further re-definitions over the years added to the list of “AIDS-defining” conditions a number of illnesses where patients often tested “HIV”-positive. This had such bizarre consequences as including tuberculosis as AIDS-defining just because TB patients often test positive for “HIV”, and including cervical cancer as “AIDS-defining” even though its incidence had been declining steadily throughout the period during which “HIV” and “AIDS” were supposedly spreading.
Then the Centers for Disease Control and Prevention decided that “HIV”-positive people with CD4-cell counts of less than 200 in the blood were to be classed as “having AIDS” even when they displayed and felt no symptoms of ill health. That criterion has not been accepted in certain other countries, however, with the result that some “AIDS” patients from the USA may cross the border into Canada and no longer have AIDS; indeed, in 1993 fully half of all newly diagnosed AIDS patients in the United States, more than 20,000 of them, could have been cured just by crossing the border.

“HIV” is variously defined as what is detected by antibody tests (ELISA or Western Blot) or by PCR detection of genetic material. ELISA and Western Blot do not always agree over whether a given sample is “positive”. The criteria for whether a Western Blot is positive are not the same in different countries nor in different laboratories. Counts of immune-system cells (CD4+) and of “viral load” (supposed amount of virus) do not correlate with one another.
Dissidents know, on the basis of any amount of documented evidence, that “HIV” tests are not specific: they react positive under many physiological conditions, and they have never been validated against pure virus, because no pure virus has ever been isolated direct from an “HIV”-positive individual.
Nevertheless, countless published articles have described “HIV” in extraordinary detail of genetic sequence and physical structure—all postulated on the basis of highly indirect inferences, since, to repeat, no single authentic particle of the virus has ever been obtained from an “AIDS” patient. All the so-called “viral isolates” stem from work with cultures; and even those are revealed by electron microscopy as motley mixtures of bits and pieces of various sizes and shapes.
An empirical and natural way of defining “HIV” is: “what HIV tests have been held to detect”. Under that view, published data from tens of millions of “HIV” tests in the United States show that “HIV” is not a sexually transmitted agent, indeed is not an infection at all, because it has been present at about the same level and in the same geographic distribution for more than two decades. The manner in which “HIV” depends on age, sex, and race indicates that it is a very non-specific physiological response to some sort of stress or health challenge. In other words, HIV/AIDS theory contradicts itself; the evidence gained by applying HIV/AIDS theory is incompatible with the theory.

4. Occasional correlations between “HIV” and “AIDS”

What makes things so exceedingly complicated and messy is that even though “HIV” and “AIDS” are not correlated in general and certainly not inevitably, as they would have to be if one were the cause of the other, there are circumstances where there is an indirect or apparent correlation between them.
Since “HIV” tests often react quite non-specifically to health stresses, people test “HIV”-positive when palpably unwell from any one of a large variety of causes; for example, “HIV”-positive rates are relatively high in hospital patients, especially those seen in emergency rooms, and among people whose deaths were such as to call for autopsies. Consequently, “HIV”-positive rates do show some sort of correlation with degree of illness in the so-called high-risk groups: drug abusers, hemophiliacs, and gay men, and this happenstance lends some apparent yet misleading support to the mainstream view.
Not acknowledged by the mainstream, but evident from mountains of data, is the fact that TB patients are another group at high risk of testing “HIV”-positive, and of course at high risk of dying as well.
Hemophiliacs suffer from a chronic, life-threatening disorder. No other explanation is required for why they test “HIV”-positive at high rates and why that sometimes appears to correlate with the severity of their illness.
Drug abusers are unhealthy or ill to varying degrees, depending on the types and amounts of drugs consumed. Addicts test “HIV”-positive because that is a response to physiological stress, and there is a consequent correlation between the degree of that drug-induced stress, that is the severity of the drug-induced ill-health, and the tendency to test “HIV”-positive. The observation that reformed drug addicts are less prone to test “HIV”-positive, in proportion to how long they have been clean, underscores that testing “HIV”-positive is in these cases an indicator of the degree of health stress, and as such it is reversible, just like a fever.
Lance’s intestinal dysbiosis article explains convincingly why gay men often test “HIV”-positive, and why that is associated with the whole spectrum of health and illness, so that there is often a correlation between the severity of the dysbiosis, the probability of testing “HIV”-positive, and the likelihood of developing “AIDS”. The intestinal-dysbiosis hypothesis also affords an explanation for the fact that the most severely ill gay men, those who experience full-blown AIDS, tend to be older rather than younger, in their thirties or forties rather than—as would be expected with a sexually transmitted disease—in their teens or twenties. Figure 10 in The Origin, Persistence and Failings of HIV/AIDS Theory shows “HIV”-positive rates among gay men aged more than 25 as higher than among younger gay men. Michelle Cochrane’s re-examination of medical records of early AIDS cases in San Francisco found that their average age was in the mid- to late thirties. The average age of the first 5 victims in Los Angeles was 31. The first 159 AIDS patients identified by the Centers for Disease Control and Prevention had an average age of 35 (pp. 187-8 in The Origin, Persistence and Failings of HIV/AIDS Theory).
Quite recently I came across yet more evidence of this correlation. A British study of “HIV”-positive gay men found that the average age of those who had no symptoms of illness was 32.4 years; those who had swollen lymph glands or other signs of what used to be called “AIDS-related complex” had an average age of 34.8; those with full-blown AIDS averaged 43.3 years of age (Batman et al., Journal of Clinical Pathology, 42 [1989] 275-81). This is precisely what the dysbiosis theory would predict: the longer one continues doing whatever causes the dysbiosis, the more likely one is to become ill.
In the same vein, a longitudinal study of gay men found that the average age of seroconverting (becoming “HIV”-positive) was 35.3 (Page-Shafer et al., American Journal of Epidemiology, 146 [1997] 531-42).
“Why are so many mid-life gay men getting HIV?”, asked Spencer Cox and Bruce Kellerhouse on GayCityNews© (15 March 2007). That’s a real conundrum under HIV/AIDS theory, but it is to be expected under intestinal-dysbiosis theory. A comment to that piece added anecdotal evidence: “… I was in my 20s and early 30s back in the 1980s and early 1990s. Although there were certainly men my age who were infected, most of the men I knew who succumbed to the epidemic in those years were 10-15 years older than I was. Most of my gay male friends in their 20s-30s were HIV negative and have remained so. I’ve spoken to several other men my age who have seroconverted later in life, and none of us lost close friends in the epidemic. But we did feel that we missed out on the ‘wild’ sex and drugs of the late 70s and early 80’s” (Jay, San Francisco, CA, Added: Tuesday March 20, 2007 at 05:47 PM EST). PLEASE NOTE APOLOGY: This quote had been incorrectly attributed to someone else up until 6 March 2009 when the error was pointed out to me.


In sum: Tony Lance’s discussion solves the main puzzles about “HIV” and “AIDS” insofar as they affect gay men, including why they have affected only a small subset of gay men. These insights are also applicable to a variety of other circumstances where disturbances of the intestinal flora have come about for one reason or another in heterosexual men and in women.
But “HIV” and “AIDS” nowadays are so different from their original connotations that many of the observations can only be explained by taking into account the continual changes in definition of both, which has enmeshed the topic of “HIV/AIDS” in a host of complications and contradictions .

Posted in HIV as stress, HIV does not cause AIDS, HIV risk groups, HIV skepticism, HIV tests, HIV varies with age | Tagged: , , , , , , , | 4 Comments »