HIV/AIDS Skepticism

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

Archive for the ‘HIV/AIDS numbers’ Category

HIV infectivity: high, low, or non-existent?

Posted by Henry Bauer on 2016/07/31

Analysis of essentially all published results of HIV tests in the USA reveals properties unlike those of an infectious agent (The Origin, Persistence and Failings of HIV/AIDS Theory, McFarland 2007).  In every social sector, the same regularities are seen: rates of testing positive vary by US official “racial” and ethnic classification (black >> native American > Caucasian > Asian); rates of testing positive decrease drastically from birth into the teens and increase from the late teens into middle age and then decline again; in early teens, females are more likely to be HIV+ than are males but by the 20s that is reversed (see references cited in section 3.3.5 in The Case against HIV).

In cloned HIV virions, only between 1 in 10,000 and 1 in 10 million were infectious (Layne et al., “Factors underlying spontaneous inactivation and susceptibility to neutralization of human immunodeficiency virus”, Virology, 189 (1992) 695-714).

The instructions that come with HIV test kits warn that a positive test is not proof of infection.

Innumerable conditions produce HIV+ results (see references cited in section 3.2 in The Case against HIV), so all claims to have measured infectivity or transmission are at best dubious and at worst — or more accurately — meaningless. There is no valid published evidence of transmission or infectivity (see references cited in section 3.3 in The Case against HIV). The Office of Medical and Scientific Justice successfully defended more than 50 individuals http://www.omsj.org/human-rights/52nd charged with transmitting HIV because the prosecution could not prove HIV to be transmissible.

Researching phantoms

It can take a long time before researchers realize that they have been on a wild-goose chase, pursuing phantoms (“Phantom phantoms”, pp. 110-116 in Fatal Attractions: The Troubles with Science, Paraview Press 2001); even “an unknown phenomenon [that] towered 6 standard deviations above the mundane background of known physics — enough to satisfy a 99.9999% confidence level that it wasn’t a fluke” and that had been reported in more than a dozen experiments turned out to be non-existent.

Given that HIV/AIDS theory is wrong (The Case against HIV), observations and experiments and clinical trials will continually throw up what seem to be conundrums, which serve as the basis for yet more research. To date, mainstream HIV/AIDS researchers have failed to recognize the accumulation of conundrums and absurdities  as being in reality the hard evidence that HIV/AIDS theory is simply wrong: HIV is not infectious, and “HIV” doesn’t cause AIDS.

Mainstream science sticks to theories that had once been accepted by ignoring anomalies, conundrums, absurdities for as long as possible (Thomas S. Kuhn, The Structure of Scientific Revolutions, University of Chicago Press 1970 [2nd ed., enlarged; 1st ed. was 1962]). Things that don’t fit an existing theory are accommodated by ad hoc adjustments (Imre Lakatos, “History of science and its rational reconstruction”, pp. 1-40 in Method and Appraisal in the Physical Sciences, ed. Colin Howson, Cambridge University Press 1976), just as Ptolemy long maintained belief in the circular perfection of heavenly motions by adding epicycles upon epicycles, wheels within wheels, to avoid acknowledging that the movements are not really circular after all.

So too HIV/AIDS researchers create new hypotheses to bolster their belief whenever they seem unable to explain what they observe. Since all the data point to HIV not being infective, or being apparently infective to so low a degree as to be incapable of producing an epidemic, auxiliary hypotheses were suggested which have become accepted as shibboleths:

  1. The epidemic in Africa is said to have come about because of an incredible rate of promiscuity. Sexually active South Africans (black South Africans, that is) are postulated to have an average of 10 sexual partners at any give time and to change them about annually (pp. 63-65 in James Chin, The AIDS Pandemic, Radcliffe 2007).
  2. Soon after initial infection, there is an “acute phase” where large amounts of HIV are present, and intercourse during that phase makes transmission much more likely: infectivity is very high during these short periods, so overall measurements of transmissibility are deceiving.

The first suggestion is absurd, since such behavior would be so visibly evident that it could not be overlooked; yet it is not observed.

The second suggestion has been undermined by a careful re-analysis of the single study on which it had been based: the “excess hazard-months attributable to the acute phase of infection” is about 5.3, not the previously estimated 31-to-141 (Bellan et al., “Reassessment of HIV-1 acute phase infectivity: accounting for heterogeneity and study design with simulated cohorts”, PLoS Medicine, 12(3):  e1001801).

HIV/AIDS research is chasing red herrings, phantoms, in a decades-long wild-goose change that has been enormously expensive in lives and in dollars. But the interests vested in this state of affairs — drug-company profits, research careers, administrative careers, honors and awards — are so widespread and powerful that the actual evidence is given little or no chance of speaking for itself. Try to imagine what it would take for Anthony Fauci to shed cognitive dissonance and admit that he has been so disastrously wrong.

 

Posted in clinical trials, experts, HIV absurdities, HIV and race, HIV does not cause AIDS, HIV tests, HIV transmission, HIV varies with age, HIV/AIDS numbers, Legal aspects, M/F ratios | Tagged: , | 16 Comments »

About money, and HIV in Estonia

Posted by Henry Bauer on 2016/02/12

A correspondent from Estonia shared this recent news:

Unique HIV is spreading in Estonia
Research has shown that recombined (?) [recombinant = hybrids of the known “strains”] form of HIV spreads in Estonia. People get infected locally and it is not brought in from abroad.
‘We have done more than 10 years of research and we do not have exporters [?importers?] of HIV, we do not get it from Russia or Western Europe’, says Irja Lutsar, professor of medical microbiology and virology. She added that people get infected with HIV locally and a recombined [recombinant] form of HIV is spreading here.
‘Our virus is unique but if you ask where it came from then I do not know answer to that.’”

Professor Lutsar might find some clues in de Harven’s article in Journal of the American Physicians and Surgeons  as well as in The Case against HIV.

“Also, US, British and Finnish embassies here recently wrote a public letter to Estonian parliament about HIV”.

Part of that letter reads;
“The U.S. President’s Emergency Plan for AIDS Relief (PEPFAR) is the largest commitment by any nation to combat a single disease. Through PEPFAR, the U.S. government works with vulnerable, developing nations on a framework to combat HIV/AIDS. Since 2009, the U.S. government has committed nearly $65 billion to support PEPFAR and its global HIV/AIDS response. While gains have been real, progress against this disease, even in the United States, has been uneven.”

That inevitably brought to mind the quote attributed to the late Republican fiscal conservative, Senator Everett Dirksen:

“A billion here, a billion there, pretty soon, you’re talking real money”.

(As commonly with the most delightful quotes, this may be a mis-attribution)

At any rate, the United States has apparently disbursed $65 billion without anyone getting any benefit and some undoubtedly being harmed as a result of being fed toxic drugs while not only healthy but even HIV-negative.
I shouldn’t have said, of course, that no one benefited. The drug companies and their shareholders and executives have certainly benefited.

 

Posted in antiretroviral drugs, Funds for HIV/AIDS, HIV absurdities, HIV risk groups, HIV skepticism, HIV tests, HIV/AIDS numbers, uncritical media | Tagged: , , | 7 Comments »

Gay genes and HIV

Posted by Henry Bauer on 2015/10/06

Some 20 years ago, Dean Hamer reported an association between certain DNA markers and being gay [1]. The report was met with considerable skepticism. Now a new study [2] has reached much the same conclusion as Hamer. This may be relevant to the apparently greater frequency of “HIV-positive” among gay men.

Overall data are clear, that “HIV-positive” does not behave like an infectious condition [3]. More specifically, if “HIV-positive” is ever transmitted sexually then it is with essentially negligible probability, according to the Centers for Disease Control & Prevention:

Heterosexual vaginal transmission is estimated as less than 1 per 1000, but receptive anal intercourse is estimated at 1.4%. This is still less by a large factor than the transmissibility of known venereal diseases like syphilis and gonorrhea. Where does the estimate originate?

It cannot be based on observations in prisons since several such studies reported much lower rates there (p. 47 in [3]). Rather, the estimate likely comes from data on “HIV-positive” among gay men who frequently practice receptive intercourse. In other words, there is a correlation between being gay, receptive anal practices, and testing “HIV-positive”. In prisons, there is a significant amount of anal intercourse by men who are not gay, yet this apparently does not correlate with becoming “HIV-positive”. Evidently it is being gay, more than anal intercourse, that correlates with being “HIV-positive”.

If there is a genetic pre-disposition to being gay, as the Hamer and Sanders studies indicate, then perhaps there is also a genetic pre-disposition among gay men to testing “HIV-positive”.

That some genetic characteristics do predispose to testing “HIV-positive” is demonstrated by racial differences. Men of sub-Saharan ancestry test “HIV-positive” at rates about 7 or 8 times greater than with Caucasian men and about 10 times greater than with Asian men. There are also racial differences in the sensitivity of “HIV” tests to the p24 protein which is one of the “HIV” markers (section 3.4 in The Case against HIV).

I’m not suggesting, of course, that genes could be the sole reason why gay men are more frequently “HIV-positive” than others. Genetic pre-dispositions are probabilistic. Not all gay men test “HIV-positive”. In the earliest days of AIDS, only a small proportion of gay men became ill. Many gay men are both “HIV-positive” and healthy and never contract “AIDS”-type diseases.
Moreover, “HIV-positive” reflects any number of possible conditions, most of which are experienced equally by gay men and everyone else (section 3.2.2 in The Case against HIV).

Similarly, the Hamer and Sanders studies do not suggest that genetics determines sexual orientation, merely that it can bring a heightened tendency; it is explicitly a small effect, to the degree that genetic studies on infants or embryos could not have any useful predictive value [2]. It is widely agreed that behavioral characteristics in general arise from some combination of hereditary and environmental factors. Moreover, it remains to compare the frequent correlation of certain genetic factors with being gay to the overall frequency of those particular factors among all men, which would indicate how strongly those factors may predispose toward a preferred sexual orientation.

So explanations for the greater incidence of “HIV-positives” among gay men are obviously and necessarily partial and multiple. I believe that some proportion of “HIV-positives” among gay men, correlated with also becoming ill, can be explained by the intestinal dysbiosis theory. Here I am suggesting that one possible and additional reason why some gay men are “HIV-positive” may be a genetic pre-disposition, particularly when “HIV-positive” does not correlate with a high probability of illness. Since the markers identified by Hamer and Sanders are not exclusive to gay men, a linkage between those markers and testing “HIV-positive” could also explain some of the incidence of “HIV-positive” among men who are not gay.
————————————
[1] Dean H. Hamer et al., “A linkage between DNA markers on the X chromosome and male sexual orientation,” Science 261 (1993) 321-7
[2] A. R. Sanders et al., “Genome-wide scan demonstrates significant linkage for male sexual orientation”, Psychological Medicine 45 (2015) 1379-88
[3] Henry H. Bauer, The Origin, Persistence and Failings of HIV/AIDS Theory, McFarland 2007

 

Posted in clinical trials, HIV and race, HIV risk groups, HIV tests, HIV transmission, HIV/AIDS numbers, sexual transmission | Tagged: , | Leave a Comment »

Antiretrovirals kill: Official data, peer-reviewed journal

Posted by Henry Bauer on 2015/08/10

(updated with full article)

HIV+ people in hospital who were on anti-retrovirals were more likely to die of non-AIDS conditions than HIV+ people NOT being treated with ARVs. The deaths were owing to known “side” effects of ARVs: cardiovascular, liver, various infections.

That is reported in the paper drawn to my attention by a comment from lukas. Note that the data covers a period of 16 years beginning with the introduction of “life-saving HAART cocktails” in the mid-1990s:

Cowell et al., TRENDS IN HOSPITAL DEATHS AMONG HUMAN IMMUNODEFICIENCY VIRUS-INFECTED PATIENTS DURING THE ANTIRETROVIRAL THERAPY ERA, 1995 TO 2011,
Journal of Hospital Medicine, 30 June 2015 doi: 10.1002/jhm.2409. [Epub ahead of print]

Here is the full paper, courtesy of David Rasnick:

Cowell 2015 copy

And here is just the abstract:

RESULTS:
In-hospital deaths declined significantly from 1995 to 2011 (P < 0.0001); those attributable to non-AIDS increased (43% to 70.5%, P < 0.0001). Non-AIDS deaths were most commonly caused by non-AIDS infection (20.3%), cardiovascular (11.3%) and liver disease (8.5%), and non-AIDS malignancy (7.8%). Patients with non-AIDS compared to AIDS-related deaths were older (median age 48 vs 40 years, P < 0.0001), more likely to be on ART (74.1% vs 55.8%, P = 0.0001), less likely to have a CD4 count of <200 cells/mm3 (47.2% vs 97.1%, P < 0.0001), and more likely to have an HIV viral load of ≤400 copies/mL (38.1% vs 4.1%, P < 0.0001). Non-AIDS deaths were associated with 4.5 and 4.2 times greater likelihood of comorbid underlying liver and cardiovascular disease, respectively.
CONCLUSIONS:
Non-AIDS deaths increased significantly during the ART era and are now the most common cause of in-hospital deaths; non-AIDS infection, cardiovascular and liver disease, and malignancies were major contributors to mortality. Higher CD4 cell count, liver, and cardiovascular comorbidities were most strongly associated with non-AIDS deaths. Interventions targeting non-AIDS-associated conditions are needed to reduce inpatient mortality among HIV-infected patients. Journal of Hospital Medicine 2015. © 2015 Society of Hospital Medicine.
© 2015 Society of Hospital Medicine.

This journal is not held by our library, and I’m waiting for Interlibrary Loan to get me a copy. IN the meantime, the abstract’s details given above seem to tell the story clearly enough.

 

Posted in antiretroviral drugs, HIV risk groups, HIV/AIDS numbers | Tagged: | 22 Comments »

HIV/AIDS history and facts

Posted by Henry Bauer on 2015/08/08

Cardiac surgeon  Donald W. Miller has written a wonderfully comprehensive yet concise analysis of the genesis of HIV/AIDS and of the actual facts:

“HIV/AIDS: Unmasking Medical Falsehood…”. 
https://www.lewrockwell.com/2015/08/donald-w-miller-jr-md/unmasking-medical-falsehood/

It illustrates the feeling of alienation, of being relatively sane in an insane world, that I get periodically:

Who looks at evidence? Almost no one
http://wp.me/p2VG42-5L

 

Posted in antiretroviral drugs, consensus, experts, Funds for HIV/AIDS, global warming, HIV absurdities, HIV does not cause AIDS, HIV risk groups, HIV skepticism, HIV tests, HIV/AIDS numbers, Legal aspects, sexual transmission, unwarranted dogmatism in science, vaccines | Tagged: , , | 4 Comments »

 
Follow

Get every new post delivered to your Inbox.

Join 128 other followers