Posted on 12/09/2007 9:42:48 AM PST by GodGunsGuts
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The dogmatic adherence to the man caused global warming hypothesis is ample evidence of how politics is manipulating good science. Fortunately there are an increasing number of studies that challenge the prevailing global warming hypothesis and in the age of the new media are not being silenced or relegated to obscurity. I would think that any reputable scientist would not want to be associated with global warming adherents who label any peer reviewed studies that disagree with their dogma to be “deniers”.
Duesberg does not need a grant to prove his theories on AIDS. All he has to do is to inject himself with HIV and show that he doesn't get AIDS. Or he can find a volunteer to do this. A number of researchers in the past have performed similar experiments. Duesberg has had 20 years to do this.
“destroys its own credibility by accepting wholesale a number of theories which are at least very questionable”
Just a comment, none of these are at the theory level, maybe not well formed hypotheses but hypotheses never the less. If you can find a volunteer to inject with HIV without going to jail and then get the results published in an ethical journal your very lucky or not in the USA.
Ethics aside, if your research does not follow the reviewers prejudices, getting it published is as hard a getting a grant in many cases. The politics of science and AIDS is down an dirty.
Let’s be sure to watch Expelled movie with Ben Stein in Feb.
Duesberg hasn't done this because the university flatly told him that if they got an inkling that he did, they would terminate his chair. But others have done it; lots of others, and none have managed to contract any more than a headache. Further, if you check on Christine Maggiore's organization, you will find that there are thousands of people that were intelligent enough to reject the stupid notion that antibodies to a harmless retrovirus could threaten their lives, and have lived happy, healthy lives, for as long as 26 years in some cases.
LOL...but largely true. Or better yet, revise or withhold data to fit prevailing orthodoxy.
==This article has some very good points at the beginning but then destroys its own credibility by accepting wholesale a number of theories which are at least very questionable, and not only because of a peer-review cabal.
I didn’t get that impression at all. What I took from the article is that said “number of theories” deserve to be explored, but are currently sitting on the backburner (if not overtly censored) because they fly in the face of “consensus” scientific opinion...and it is these very consensus scientists who close ranks against non-consensus scientists by spiking their grant and paper proposals.
I'll take your word for it that that is his excuse.
But others have done it; lots of others, and none have managed to contract any more than a headache.
Name one.
By the way, how do you explain the thousands of hemophiliacs in the US who contracted HIV before testing of blood products began and subsequently died of AIDS?
Further, if you check on Christine Maggiore's organization, you will find that there are thousands of people that were intelligent enough to reject the stupid notion that antibodies to a harmless retrovirus could threaten their lives, and have lived happy, healthy lives, for as long as 26 years in some cases.
Too bad that didn't work out for Maggiore's own daughter. I think I'll believe that opinion of the LA coroner who said that Maggiore's daughter died of untreated AIDS, rather than Maggiore, who has no scientific training. It's sad that this poor little girl had to die because of her mother's stupidity.
BTW, it is not antibodies that threatens the lives of people with AIDS.
There is no such thing as “dying of AIDS.”
People that “die of AIDS” die of TB, or Pnuemonia usually.
That's like saying that being in a car accident is not a legitimate cause of death because it's the loss of blood and decapitation that kills you. It is certainly not healthy to have a non-functional immune system.
No, in most cases, TB is the only disease that they have. TB is normally a slow killer, if it kills at all, but those that use the ‘poppers’ and other dialators that are common in the gay sex scene have no immune response. This is actually equally true whether they happen to have HIV anti-bodies or not. The deaths are equally distributed between HIV+ and HIV-. Sometimes the TB doesn’t get to be the ultimate culpret; it can be pnuemonia, or staph, which are common in hospitals and rest homes.
Actually, even though 75% of hemophiliacs were HIV+, the mortality rate of hemophiliacs had been decreasing all the way up to 1987. Thus, one could make the seemingly logical but obviously fallacious argument that HIV prolonged the life of hemophiliacs. As for the sudden spike in hemophiliac mortality after 1987, Duesberg, Koehnlein and Rasnick point to the introduction of the highly toxic chemotherapy drug AZT:
Here, we present evidence that anti-HIV drugs cause
AIDS defining diseases, other diseases and death, both (i)
in the presence and (ii) in the absence of HIV.
(i) Diseases and death in HIV-positives treated with anti-
HIV drugs: A sudden 10-fold increase in the mortality of
HIV-positive British hemophiliacs, right after the introduction of AZT in 1987, made scientific headlines in
1995, because the increased mortality was attributed to
HIV by the authors of the study, i.e. Darby et al (1995),
as well as by the editor of Nature, “More conviction on
HIV and AIDS” (Maddox 1995). Even the editor of the
Lancet wrote an editorial asking, “Will Duesberg now
concede defeat” (Horton 1995)? Darby et al based their
conclusion on the sudden 10-fold increase of the hemophiliacs’ mortality in 1987, shown in figure 5, on the
facts that the increased mortality was restricted to HIVpositive hemophiliacs and that the increase was independent of the degree of hemophilia (which is inversely
proportional to the life expectancy of the patient).
But, by 1987 transfusions of blood and factor VIII had
already infected most hemophiliacs for a long time. Most
of them were already infected before 1984 (about 75% in
the US), because all blood supplies with HIV antibodies
were banned after the introduction of the HIV-antibody test in 1984 (Duesberg 1995c, 1996a). Moreover, the
mortality of hemophiliacs was steadily decreasing since
the 1970s until 1987 – despite the presence of HIV
(Duesberg 1995c)! Thus the only new risk of mortality,
in and after 1987, was not HIV, but AZT. Darby et al
even acknowledged “treatment, by prophylaxis against
P. carinii pneumonia or with zidovudine (AZT), has
been widespread for HIV-infected haemophiliacs since
about 1989 (more accurately since 1987)”. The editor
of Nature also pointed out that, “Darby et al failed to
provide full details of the drug regimen followed” (Maddox 1995). The AZT-mortality hypothesis would of
course also explain why the new hemophilia mortality
was independent of the severity of the hemophilia, as
Darby et al observed. Nevertheless Nature, did not accept
an alternative interpretation, specifically not from “Those
who have made the running in the long controversy over
HIV in AIDS, Dr Peter Duesberg of Berkeley, California,
in particular . . .” (Maddox 1995). But, the Lancet accepted a response, which proposed that AZT treatments were the probable cause of the sudden increase in mortality of hemophiliacs (Duesberg 1995d).
According to researchers from the NIH, AZT also increased
the mortality of US hemophiliacs 2×7 times and
their AIDS risk 4×5 times compared to untreated controls
(Goedert et al 1994; Duesberg 1995c). The medical literature describes many more examples of AIDS defining,
other diseases and deaths that developed in HIV-positive
asymptomatic people or in AIDS patients treated with
anti-HIV drugs, which were not observed in untreated
controls; some of these are summarized in table 6.
The death rate for hemophiliacs in the US suddenly increased in the first quarter of 1984 and kept rising for several years after that. AZT wasn't licensed until 1987.
See graph on first page here.
Apparently Duesberg at first claimed that the AIDS-related deaths in hemophiliacs was due to their use of Factor VIII. After studies showed that the death rate was independent of the amount of Factor VIII used, he started blaming AZT. But that doesn't seem to square with this graph from the CDC.
Not correct:
Duesberg on Hemophilia and AIDS:
3.4.4.5. HIV-positive hemophiliacs. The hemophiliacs provide the most accessible group to test the virus hypothesis, because the time of infection can be estimated and because the role of other health risks can be controlled by studying HIV-free hemophiliacs.
About 15,000, or 75% of the 20,000 American hemophiliacs have HIV from transfusions received before the “AIDS test” was developed in 1984 (Tsoukas et al., 1984; Hardy et al., 1985; Institute of Medicine, 1986, 1988; Stehr-Green et al., 1988; Goedert et al., 1989; Koerper, 1989). Based on limited data and antibodies against selected viral antigens, it is generally estimated that most of these infections occurred between 1978 and 1984 (Evatt et al., 1985; Johnson et al., 1985; McGrady et al., 1987; Goedert et al., 1989). This high rate of infection reflects the practice, developed in the 1960s and 1970s, of preparing factor VIII from blood pools collected from large numbers of donors (Johnson et al., 1985; Aronson, 1988; Koerper, 1989). Since only about 300 of the 15,000 HIV-infected American hemophiliacs have developed AIDS annually over the last 5 years (Morgan et al., 1990; Centers for Disease Control, 1992a,b), the annual AIDS risk of HIV-infected American hemophiliacs is about 2% (Table 2). Data from Germany extend these results: about 50% of the 6000 German hemophiliacs are HIV-positive (Koerper, 1989), and only 37 (1%) of these developed AIDS-defining diseases during 1991 and 303 (1% annually) from 1982 until 1991 (Bundesgesundheitsamt (Germany), 1991; Leonhard, 1992). An international study estimated the annual AIDS risk of adult hemophiliacs at 3% and that of children at 1% over a 5-year period of HIV-infection (Biggar and the International Registry of Seroconverters, 1990).
According to the virus-AIDS hypothesis, one would have expected that by now (about one 10-year-HIV-latent-period after infection) at least 50% of the 15,000 HIV-positive American hemophiliacs would have developed AIDS or died from AIDS. But the 2% annual AIDS risk indicates that the average HIV-positive hemophiliac would have to wait for 25 years to develop AIDS diseases from HIV, which is the same as their current median age. The median age of American hemophiliacs has increased from 11 years in 1972, to 20 years in 1982 and to over 25 years in 1986, despite the infiltration of HIV in 75% (Johnson et al., 1985; Institute of Medicine, 1986; Koerper, 1989). Thus, one could make a logical argument that HIV, instead of decreasing the lifespan of hemophiliacs, has in fact increased it.
Considering the compromised health of many hemophiliacs compared to the general population, it is also surprising, that the 1-2% annual AIDS risk of HIV-infected hemophiliacs is lower than the 3-4% risk of the average HIV-infected, nonhemophilic European or American (Table 1). There is even a bigger discrepancy between the annual AIDS risks of hemophiliacs and those of intravenous drug users and male homosexuals, which are both about 4-6% (Table 2). In an effort to reconcile the relatively low annual AIDS risks of hemophiliacs with that of homosexuals, the hematologists Sullivan et al. (1986) noted “The reasons for this difference remain unclear.” And Biggar and colleagues (1990) noted that “AIDS incubation ... was significantly faster” for drug users and homosexuals than for hemophiliacs.
In view of the many claims that HIV causes AIDS in hemophiliacs, it is even more surprising that there is not even one controlled study from any country showing that the morbidity or mortality of HIV-positive hemophiliacs is higher than that of HIV-negative controls.
Instead, controlled studies show that immunodeficiency in hemophiliacs is independent of HIV, and that the lifetime dosage of transfusions is the cause of AIDS-defining diseases of hemophiliacs. Studies describing immunodeficiency in HIV-free hemophiliacs are summarized in Table 3 (Tsoukas et al., 1984; AIDS Hemophilia French Study Group, 1985; Ludlam et al., 1985; Gill et al., 1986; Kreiss et al., 1986; Madhok et al., 1986; Sullivan et al., 1986; Sharp et al., 1987; Matheson et al., 1987; Antonaci et al., 1988; Mahir et al., 1988; Aledort, 1988; Jin et al., 1989; Jason et al., 1990; Lang, et al., 1989; Becherer et al., 1990). One of these studies even documents an AIDS-defining disease in an HIV-free hemophiliac (Kreiss et al., 1986). Immunodeficiency in these studies is typically defined by a T4 to T8-cell ratio of about 1 or less than 1, compared to a normal ratio of 2.
Most of the studies listed in Table 3 and additional ones conducted before HIV had been discovered have concluded or noted that immunodeficiency is directly proportional to the number of transfusions received over a lifetime (Menitove et al., 1983; Kreiss et al., 1984; Johnson et al., 1985; Hardy et al., 1985; Pollack et al., 1985; Prince, 1992; Ludlum et al., 1985; Gill et al., 1986). According to the hematologists Pollack et al. (1985) “derangement of immune function in hemophiliacs results from transfusion of foreign proteins or a ubiquitous virus rather than contracting AIDS infectious agent.” The “ubiquitous virus” was a reference to the virus-AIDS hypothesis but a rejection of HIV, because in 1985 HIV was extremely rare in blood concentrates outside the U.S., but immunodeficiency was observed in Israeli, Scottish and American hemophiliacs (Pollack et al., 1985). Madhok et al. also arrived at the conclusion that “clotting factor concentrate impairs the cell mediated immune response to a new antigen in the absence of infection with HIV” (Madhok et al., 1986). Aledort observed that “chronic recipients ... of factor VIII, factor IX and pooled products ... demonstrated significant T-cell abnormalities regardless of the presence of HIV antibody” (Aledort, 1988). Even those who claim that clotting factor does not cause immunodeficiency show that immunodeficiency in hemophiliacs increases with both the age and the cumulative dose of clotting factor received during a lifetime (Becherer et al., 1990).
One controlled study showed directly that protein impurities of commercial factor VIII, rather than factor VIII or HIV, were immunosuppressive among factor VIII-treated, HIV-positive hemophiliacs. Over a period of two years the T-cells of HIV-positive hemophiliacs treated with commercial factor VIII declined two-fold, while those of matched HIV-positive controls treated with purified factor VIII remained unchanged (Table 3) (de Biasi et al., 1991).
Before AIDS, a multicenter study investigating the immune systems of 1551 hemophiliacs treated with factor VIII from 1975 to 1979 documented lymphocytopenia in 9.3% and thrombocytopenia in 5% (Eyster et al., 1985). Accordingly, AIDS-defining opportunistic infections, including 60% pneumonias and 20% tuberculosis, have been recorded in hemophiliacs between 1968 and 1979 (Johnson et al., 1985). These transfusion-acquired immunodeficiencies could more than account for the 2% annual incidence of AIDS-defining diseases in HIV-positive hemophiliacs recorded now (Centers for Disease Control, 1992b). An American hematologist who recorded opportunistic infections in hemophiliacs occurring between 1968 and 1979, including 2 candidiasis and 66 pneumonia deaths, commented in 1983 “... it seems possible that many of the unspecified pneumonias in hemophiliacs in the past would be classified today as AIDS” (Aronson, 1983).
It follows that long-term transfusion of foreign proteins causes immunodeficiency in hemophiliacs with or without HIV. The virus hypothesis has simply claimed normal morbidity and mortality of hemophiliacs for HIV, by ignoring HIV-free controls.
Nevertheless several investigators comparing HIV-negative to HIV-positive hemophiliacs have noted that immunodeficiency is more often associated with HIV-positives (Table 3), and have observed that HIV correlates with the number of transfusions received (Tsoukas et al., 1984; Kreiss et al., 1986; Sullivan et al., 1986; Koerper, 1989; Becherer et al., 1990). According to Kreiss et al. “seropositive hemophiliac subjects, on average, had been exposed to twice as much concentrate ... as seronegative[s]” (Kreiss et al., 1986). And according to Goedert et al. “the prevalence of HIV-1 antibodies was directly associated with the degree of severity (of hemophilia)” (Goedert et al., 1989). Thus HIV appears just to be a marker of the multiplicity of transfusions, rather than a cause of immunodeficiency.
The conclusion that long-term transfusion of foreign proteins causes immunodeficiency makes three testable predictions:
(1) It predicts that hemophiliacs with “AIDS” would be older than average hemophiliacs. Indeed, the median age of hemophiliacs with AIDS in the U.S. (Evatt et al., 1984; Koerper, 1989; Stehr-Green et al., 1989), England (Darby et al., 1989) and other countries (Biggar and the International Registry of Seroconverters, 1990; Blattner, 1991) is significantly higher (about 34 years in the U.S.; Johnson et al., 1985; Koerper, 1989; Becherer et al., 1990) than the average age of hemophiliacs (20-25 years in the U.S., see above). Goedert et al. reported that the annual AIDS risk of 1- to 17-year-old hemophiliacs was 1.5%, that of 18- to 34-year-old hemophiliacs was 3% and that of 64-year-old hemophiliacs was 5% (Goedert et al., 1989). This confirms that the cumulative dose of transfusions received is the cause of AIDS-defining diseases among hemophiliacs. According to the hematologist Koerper, “this may reflect lifetime exposure to a greater number of units of concentrate, ...” and to Evatt et al., “This age bias may be due to differences in duration of exposure to blood products ...” (Evatt et al., 1984; Koerper, 1989).
By contrast, AIDS caused by an autonomous infectious pathogen would be largely independent of the age of the recipient. Even if HIV were that pathogen, the hemophiliac population with AIDS should have the same age distribution as the hemophiliac population over 10 years, because HIV is thought to take 10 years to cause AIDS and nearly all hemophiliacs were infected about 10 years ago (Johnson et al., 1985; McGrady et al., 1987; Koerper, 1989).
(2) Foreign protein-mediated immunodeficiency further predicts that all AIDS diseases of hemophiliacs are opportunistic infections. If hemophilia AIDS were due to HIV only 62% of their AIDS diseases would be opportunistic infections, because 38% of all American AIDS patients have diseases, that are not dependent on, and not consistently associated with, immunodeficiency (Table 1, Section 3.5.8). These include wasting disease (19%), Kaposi’s sarcoma (10%), dementia (6%) and lymphoma (3%) (Table 1).
The AIDS pathology of hemophiliacs confirms the prediction of the foreign protein-hypothesis exactly. In America 99% of the hemophiliacs with AIDS have opportunistic infections, of which about 70% are fungal and viral pneumonias, and less than 1% have Kaposi’s sarcoma (Evatt et al., 1984; Selik et al., 1987; Stehr-Green et al., 1988; Goedert et al., 1989; Koerper, 1989; Becherer et al., 1990). The small percentage of Kaposi’s sarcoma is due to the nitrite inhalants used by male homosexual hemophiliacs as sexual stimulants (Section 4). There are no reports of wasting disease and dementia in hemophiliacs.
(3) If hemophilia AIDS is due to transfusion of foreign proteins, the wives of hemophiliacs should not contract AIDS from their mates. But if it were due to a parenterally or sexually transmitted virus, hemophilia AIDS would be sexually transmissible. Indeed, AIDS researchers claim that the wives of hemophiliacs develop AIDS from sexual transmission of HIV (Lawrence et al., 1990; Weiss and Jaffe, 1990; Centers for Disease Control, 1992b). For example AIDS researcher Fauci asks: “How about the 60-year-old wife of a hemophiliac who gets infected? Is she cruising, too?” (Booth, 1988).
However, (a) statistical scrutiny and (b) a controlled study unconfirm the hypothesis that hemophilia AIDS is sexually transmissible: (a) The CDC reports that 94 wives of hemophiliacs have been diagnosed with unnamed AIDS diseases since 1985 (Centers for Disease Control, 1992b). If one considers that there have been 15,000 HIV-positive hemophiliacs in the U.S. since 1985 and assumes that a third are married, then there are 5000 wives of HIV-positive hemophiliacs. About 13 of these women have developed AIDS annually during the 7 years (94:7) from 1985 to 1991 (Centers for Disease Control, 1992b). By contrast, at least 80 of these women would be expected to die per year, considering the human lifespan of about 80 years and that on average at least 1.6% of all those over 20 years of age die annually. Thus, until controls show that among 5000 HIV-negative wives of hemophiliacs only 67 (80-13) die annually, the claim that wives of hemophilics die from sexual transmission of HIV is unfounded speculation.
Moreover, it has been pointed out that all AIDS-defining diseases of the wives of hemophiliacs are typically age-related opportunistic infections, including 81% pneumonia (Lawrence et al., 1990). Kaposi’s sarcoma, dementia, lymphoma and wasting syndrome are not observed in wives of hemophiliacs (Lawrence et al., 1990). Thus the virus-AIDS hypothesis seems to claim, once more, normal morbidity and mortality of the wives of hemophiliacs for HIV.
(b) To test the hypothesis that immunodeficiency of hemophiliacs is sexually transmissible the T4 to T8 cell-ratio of 41 spouses and female sexual partners of immunodeficient hemophiliacs were analyzed (Kreiss et al., 1984). Twenty-two of the females had relationships with hemophiliacs with T-cell ratios below 1 and 19 with hemophiliacs with ratios of 1 and greater. The mean duration of relationships was 10 years, the mean number of sexual contacts was 111 during the previous year, and only 12% had used condoms (Kreiss et al., 1984). Since the T-cell ratios of all spouses were normal, averaging 1.68-exactly like those of 57 normal controls, the authors concluded that “there is no evidence to date for heterosexual or household-contact transmission of T-cell subset abnormalities from hemophiliacs to their spouses ...” (Kreiss et al., 1984).
It follows that the foreign protein-hypothesis, but not the HIV-hypothesis, correctly predicts (1) the pathology, (2) the age bias, (3) the noncontagiousness of hemophilia AIDS and (4) HIV-free immunodeficiency in hemophiliacs. It also explains the discrepancies between the annual AIDS risks of hemophiliacs and other risk groups (Table 2).
Since the virus hypothesis has become totally dominant in 1988, no new studies have described HIV-free immunodeficient hemophiliacs (Table 3) and the question whether HIV-free immunodeficient hemophiliacs ever developed AIDS-defining diseases became a taboo. The study by Jason et al. described data collected in the mid 1980s, the studies by Jin et al. and Becherer et al. collected data before 1988 and the one by de Biasi et al. compared the effects of purified to unpurified factor VIII only in HIV-positive hemophiliacs (Table 3).
In response to the argument that hemophiliacs only began to develop AIDS diseases when HIV appeared (Centers for Disease Control, 1986; Oppenheimer, 1992), it is proposed that “new” AIDS-defining diseases among hemophiliacs are an indirect consequence of extending their life with factor VIII treatment. Long-term treatment with factor VIII has prolonged the median life of hemophiliacs from 11 in 1972 to 25 in 1986. But contaminating foreign proteins received over periods of 10 years of treatment have also caused immunodeficiencies, and various viral and microbial contaminants have caused infections in some, and HIV infection in 75%. HIV has been a marker for the number of transfusions and factor VIII treatments received, just like hepatitis virus infection was a marker of the number of transfusions received until it was eliminated from the blood supplies (Anonymous, 1984; Koerper, 1989). Prior to factor VIII therapy most hemophiliacs died as adolescents from internal bleeding (Koerper, 1989).
http://www.duesberg.com/papers/ch62-2.html
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