The Government Grant System (Twisting science to serve the state)

Flush with success in creating an atom bomb, the U.S. federal government decided it should start funding nonmilitary scientific research. A government report titled "Science, the Endless Frontier" provides the justification for doing this. It makes the case that "science is the responsibility of government because new scientific knowledge vitally affects our health, our jobs, and our national security" (Bush, 1945). Accordingly, the government established a Research Grants Office in January, 1946 to award grants for research in the biomedical and physical sciences. It received 800 grant applications that year. The Research Grants Office is now known as the Center for Scientific Review (CSR), and it processes applications submitted to the National Institutes of Health (NIH) and other agencies in the U.S. Department of Health and Human Services (HHS). In 2005 CSR received 80,000 grant applications.

Investigators seeking an NIH grant submit a 25-page Research Plan that begins with an abstract placed in a half-page box on the form. The Specific Aims of the project, preferably two to four, come next (recommended length, 1 page). The applicant must show that these objectives are attainable within a stated time frame. As one NIH center (the National Cancer Institute) advises in its online Guide for Grant Applications, "A small, focused project is generally better received than a diffuse, multifaceted project." The other components of the Research Plan are Background and Significance (3 pages); Preliminary Studies the applicant has done (6-8 pages); Research Design and Methods (about 15 pages); and, if applicable, Human Subjects and Vertebrate Animals considerations. The investigator must also submit a detailed budget for the project on a separate form.

The Center for Scientific Review "triages" applications it receives. A cursory appraisal eliminates one-third of the applications from any further consideration, and it selects the remaining two-thirds for competitive peer review. CSR sends each application to a Study Section it deems best suited to evaluate it. Peers in Molecular Oncogenesis, Cognitive Neuroscience, Cell Structure and Function, Hematopoiesis, HIV/AIDS Vaccine, and 167 other Study Sections review grant applications. Each Study Section has 12-24 members who are recognized experts in that particular field. Members meet three times a year to review 25-100 grants at each meeting. Two members read an application and then discuss it with the other section members who collectively give it a priority score and percentile ranking (relative to the priority scores they assign to other applications). An advisory council then makes funding decisions on the basis of the Study Section’s findings, "taking into consideration the [specific NIH] institute or center’s scientific goals and public health needs" (Scarpa, 2006). CSR’s slogan is "Advancing Health through Peer Review."

With a budget of $28 billion, the director of NIH reports that it currently funds 22 percent of all the grant applications it reviews (Zerhouni, 2006). Among these, multi-year R01 grants are the mainstay of research by medical school faculties. And in 2005, the NIH funded only one in eleven (9.1%) of the unsolicited R01 research grant applications it reviewed (Mandel and Vesell, 2006). In 1998 the NIH funded 31 percent of its grant applications, and since 2003 grant appropriations have lagged behind inflation (Zerhouni, 2006). The National Science Foundation awards $6 Billion in grants each year. This independent federal agency funds 28 percent of the 40,000 annual grant proposals it receives.

Twenty-six federal granting agencies now manage 1,000 grant programs. Even clinical trials of drugs, vaccines, and devices, where industry may profit from the outcome, have come under the purview of government. Zarin and colleagues (2005) reviewed ClinicalTrials.gov records and found that the federal government currently funds 9,796 (51%) of the 19,355 interventional trials being conducted. Industry sponsors 4,734 (24%); and universities, foundations, and other organizations, 4,825 (25%).

Under the current system scientists are expected to spend time drafting, writing, and refining unsolicited R01 grant applications, despite a less than one in ten chance of success.

Ethics in science and society "describe appropriate behavior according to contemporary standards" (Friedman, 1996). Two standards that scientists follow for writing grant proposals are: 1) Keep it safe and survive, and 2) Don’t lie if you don’t have to.

Pollack (2005) addresses the first ethic, noting that the paramount motivational factor for scientists today is the competition to survive. A scientist’s most pressing need, which supersedes the scientific pursuit of truth, is to get her grant funded – to pay her salary and that of her staff, to pay department bills, and to obtain academic promotion. The safest way to generate grants is to avoid any dissent from orthodoxy. Grant-review Study Sections whose members’ expertise and status are tied to the prevailing view do not welcome any challenge to it. A scientist who writes a grant proposal that dissents from the ruling paradigm will be left without a grant. Speaking for his fellow scientists Pollack writes, "We have evolved into a culture of obedient sycophants, bowing politely to the high priests of orthodoxy."

Applicants following the ethic of "keep it safe and survive" propose research that will please the reader-peers and avoid projects that might displease them. An NIH pamphlet on grant applications reinforces such behavior by stating, "The author of a project proposal must learn all he can about those who will read his proposal and keep those readers constantly in mind when he writes." (Ling, 2004a).

With regard to the second ethic, Albert Szent-Györgyi said, "I always tried to live up to Leo Szilard’s commandment, ‘don’t lie if you don’t have to.’ I had to. I filled up pages with words and plans I know I would not follow. When I go home from my laboratory in the late afternoon, I often do not know what I am going to do the next day. I expect to think that up during the night. How could I tell them what I would do a year hence?" (Moss, 1988, p.217). This long-time cancer researcher, discoverer of vitamin C, and Nobel laureate was unable, despite multiple attempts, to obtain a government grant.

Friedman (1996) describes a variant of this ethic where an investigator applies for a grant to do a study that he has already completed. With this grant awarded and money in hand he publishes the study and uses the funds on a different project. The misrepresentation enables the investigator to remain one project ahead of his funding. Apparently enough seasoned investigators do this that the academic community views the practice as sound "grantsmanship."

When the peer review grant system was established in 1946 people assumed that scientific progress occurs in an evolutionary incremental and cumulative fashion. Having a panel of experts judge the worth of each research proposal seeking funds seemed then to be the best way to allocate federal tax dollars for research. This system assumes that a majority of specialists in a given field will know where truth lies and how best to get there and find it (Ling, 2004b). But as Hall (1954) and Kuhn (1962) later showed, periodic upheavals and revolutions in science disrupt an otherwise steady growth of scientific knowledge. Long-cherished ideas are replaced wholesale by new ones that lead science in a different direction.

The grant system fosters an Apollonian approach to research. The investigator does not question the foundation concepts of biomedical and physical scientific knowledge. He sticks to the widely held belief that the trunks and limbs of the trees of knowledge, in, for example, cell physiology and on AIDS, are solid. The Apollonian researcher focuses on the peripheral branches and twigs and develops established lines of knowledge to perfection. He sees clearly what course his research should take and writes grants that his peers are willing to fund. Forced by the existing grant system to follow such an approach, Pollack (2005) argues that scientists have defaulted into becoming a culture of believers without rethinking the fundamentals.

Intuitive geniuses, like Thomas Edison, Louis Pasteur, Ernest Rutherford, and Albert Einstein, take a Dionysian, transformational approach to science. Their research relies on intuition and "accidental" discoveries. Szent-Györgyi describes intuition as "a sort of subconscious reasoning, only the end result of which becomes conscious." The Dionysian scientist knows the direction he wants to follow into the unknown, but "he has no idea what he is going to find there or how he is going to find it. Defining the unknown or writing down the subconscious is a contradiction in absurdum." And, citing Pasteur, who said, "A discovery is an accident finding a prepared mind," Szent-Györgyi notes that "accidental" discoveries are rarely true accidents (Moss, 1988, pp. 216-217).

Although it is the Dionysian method of research that produces transformative scientific breakthroughs, peers possessing the power to judge grants do not support this kind of research. They abuse the trust and power of government, which does not know science, to advance their own careers and, in some cases, protect their investments in companies that profit from the reigning paradigm. Knowing this government might be more amenable to supporting potentially transformative, Dionysian research.

To make matters worse, this system is replacing other sources of funding that formerly supported Dionysian scientists. Ling (2004b) observes, "Oversupply of scientists, the rising cost of living and of research, the decline of private foundations and scientific niches which these foundations once sustained [has] completed the dismantling of the socio-economic environment which once protected revolutionary scientists and their young followers."

Paradigms in the biomedical and climate sciences that have achieved the status of dogma are:

Cholesterol and saturated fats cause coronary artery disease. Mutations in genes cause cancer. Human activity is causing global warming through increased CO2 emissions. A virus called HIV (human immunodeficiency) causes AIDS (acquired immune deficiency syndrome). The damaging effects of toxins are dose-dependent in a linear fashion down to zero. Even a tiny amount of a toxin, such as radiation or cigarette smoke, will harm some people. The membrane-pump theory of cell physiology based on the concept that cells are aqueous solutions enclosed by a cell membrane. Scientists that question these state-sanctioned paradigms are denied grants and silenced (Moran 1998). But valid questions nevertheless have been raised about each of these established orthodoxies.

The idea that cholesterol causes coronary heart disease is now close to being dogma, and investigators that question the lipid hypothesis need not apply for funding. But there is growing evidence that the hypothesis is wrong, as Ravnskov (2000) documents in The Cholesterol Myths.

Aneuploidy (an abnormal number and balance of chromosomes), instead of mutation-produced oncogenes, may well prove to be the true cause of cancer (Bialy, 2004; Duesberg and Rasnick, 2000; Miller, 2006).

The human-caused global-warming paradigm is most likely false (Soon et al., 2001; Editorial, 2006). Two climate astrophysicists, Willie Soon and Sallie Baliunas, present evidence that shows the climate of the 20th century fell within the range experienced during the past 1,000 years. Compared with other centuries, it was not unusual (Soon and Baliunas, 2003). Unable to obtain grants from NASA (National Aeronautics and Space Administration), Soon (personal communication, August 31, 2006) observes that NASA funds programs mainly on social-political reasoning rather than science.

Duesberg (1996), Hodgkinson (2003), Lang (1993-2005), Liversidge (2001/2002), Maggiore (2000), and Miller (2006), among others, have questioned the germ theory of AIDS. All 30 diseases (which includes an asymptomatic low T-cell count) in the syndrome called AIDS existed before HIV was discovered and still occur without antibodies to this virus being present. At a press conference in 1984 government officials announced that a newly discovered retrovirus, HIV, is the probable cause of AIDS, which at that time numbered 12 diseases (Duesberg, 1995, p. 5). Soon thereafter "HIV causes AIDS" achieved paradigm status. But, beginning with Peter Duesberg, Professor of Molecular and Cell Biology at the University of California, Berkeley, a growing number of scientists, physicians, investigative journalists, and HIV positive people have concluded that HIV/AIDS is a false paradigm. The NIH awarded Duesberg a long-term Outstanding Investigator Grant and a Fogarty fellowship to spend a year on the NIH campus studying cancer genes, and he was nominated for a Nobel Prize. When Duesberg publicly rejected the HIV/AIDS paradigm the NIH and other funding agencies ceased awarding him grants. Government-appointed peer reviewers have rejected his last 24 grant applications. Peter Duesberg (personal communication, September 20, 2006) writes: When I was the blue-eyed boy finding oncogenes and "deadly" viruses, I was 100% fundable. Since I questioned the HIV-AIDS hypothesis of the NIH's Dr. Gallo, and then the cancer-oncogene hypothesis of Bishop-Varmus-Weinberg-Vogelstein etc. I became 100% unfundable. I was transformed from a virus- and cancer-chasing Angel to ‘Lucifer’."

Rather than being harmful, as predicted by the linear no threshold hypothesis, low doses of radiation are actually beneficial (Calabrese, 2005; Hiserodt, 2005). Its beneficial effect is based on hormesis, where radiation in small doses stimulates immune system defenses, prevents oxidative DNA damages, and suppresses cancer. The dose must exceed a certain threshold to stop having a simulative and start having an inhibitory effect on the body and become toxic – and in high doses, fatal (Miller, 2004).

Research in cell physiology is based on the concept that the cell, the basic structural unit that makes up all living things, is an aqueous solution of chemicals enclosed within a cell membrane. Drug research adheres to the concept that a drug’s action is mediated by fitting into a specific receptor site on the cell membrane. Ling (2001) and Pollack (2001), however, make a strong case that the membrane paradigm of cell physiology is wrong. They show that cell function does not depend on the integrity of the cell membrane, and membrane pumps and channels are not what they seem. These investigators hypothesize that the three main components of a living cell – proteins, water, and potassium ions – are structured together in a gel-like matrix, where the cell’s water is organized into layers alongside proteins. Magnetic Resonance Imaging (MRI) is a product of this view of cell physiology, known as the association-induction hypothesis, which was first proposed by Gilbert Ling in 1962. For more than 45 years government granting agencies, guided by their "expert" peer-reviewers’ verdicts, have refused to provide funds for this pioneering investigator to pursue research on this hypothesis, even after it brought about the important medical technology of MRI (Ling 2004b). Despite multiple attempts, Gerald Pollack (personal communication, September 13, 2006) also has been unable to obtain government grants to conduct research on this alternative hypothesis of cell physiology.

Peer review enforces state-sanctioned paradigms. Pollack (2005) likens it to a trial where the defendant judges the plaintiff. Grant review panels defending the orthodox view control the grant lifeline and can sentence a challenger to "no grant." Deprived of funds the plaintiff-challenger is forced to shut down her lab and withdraw. Conlan (1976) characterizes the peer-review grant system as an "incestuous ‘buddy system’ that stifles new ideas and scientific breakthroughs."

Science is self-correcting and, in time, errors are eliminated, or so we are taught. But now with a centralized bureaucracy controlling science, perhaps this rhetoric is "just wishful thinking" (Hillman, 1996, p.102). Freedom to dissent is an essential ingredient of societal health. Braben (2004) contends that suppressing challenges to established orthodoxy sets a society on a path to its doom.

Over the last 60 years a new power structure, the state, has taken control of information. It uses federal tax money to fund and control research through the peer-review grant system. It forms mutually advantageous partnerships with industry and the academic community, which do its bidding. The state holds sway over education. And to round out its control of information an increasingly powerful centralized government bureaucracy has persuaded the mainstream media to accept and espouse state-approved ideas. The Western tradition of information ethics dating from ancient Greece to the 20th century, characterized by freedom of speech and inquiry, has been co-opted by government. Knowledge advances by questioning accepted paradigms (Hillman, 1995). The state thwarts this and requires its tax-funded scientists to conform to the official establishment view on such things as global warming and HIV/AIDS.

Government-sponsored scientific research reflects the biases, preferences, and priorities of its leaders (Moran, 1998). The state uses science to further its social and political purposes.

Its actions follow Lang’s First Law of Sociodynamics, where "The power structure does what they want, when they want; then they try to find reasons to justify it. If this does not work, they stonewall it (Lang, 1998, p. 797).

When inconvenient facts challenge paradigms the state promotes, it justifies them by consensus. If polar bear experts (Amstrup et al., 1995) find that the bear population in Alaska is increasing, placing doubt on the government’s stance on climate change, this finding is dismissed as being outside the consensus and ignored. Science magazine supports the prevailing view, stating, "There is a scientific consensus on the reality of anthropogenic climate change" that accounts for "most of the observed warming over the last 50 years" (Oreskes, 2004).

In 21st century America, consensus and computer models masquerade as science. They supplant experimental data. As Corcoran (2006) puts it, "Science has been stripped of its basis in experiment, knowledge, reason and the scientific method and made subject to the consensus created by politics and bureaucrats." Reduced to a belief system, a majority of scientists and groups like the Intergovernmental Panel on Climate Change can declare, without having to provide scientific evidence, that they believe humans cause global warming. This alone makes the hypothesis become an established fact and received knowledge (Barnes, 1990). Peer review compounds the problem. It competes with objective evidence as proof of truth.

Computer models purporting to make sense of complex data, particularly with regard to climate change, have replaced the scientific goal of supplanting complicated hypotheses with simpler ones (Pollack, 2005). Researchers offer computer models as evidence for global warming. When unsound assumptions and faulty data render one model unreliable, other improved ones are constructed to justify the state’s desire to promulgate this "truth," which it can use to exert greater control over the economy and technological progress.

AIDS research serves the interest of the state by focusing on HIV as an equal opportunity cause of AIDS. This infectious, egalitarian cause exempts the two primary AIDS risk groups, gay men and intravenous drug users, from any blame in acquiring this disease(s) owing to their behavioral choices. Duesberg, Koehnlein, and Rasnick (2003) hypothesize that AIDS is caused by three other things, singly or in combination, rather than HIV: 1) long-term, heavy-duty recreational drug use – cocaine, amphetamines, heroin, and nitrite inhalants; 2) antiretroviral drugs doctors prescribe to people who are HIV-positive – DNA chain terminators, like AZT, and protease inhibitors; and 3) malnutrition and bad water, which is the cause of "AIDS" in Africa. HIV/AIDS has become a multibillion-dollar enterprise on an international level. Government, industry, and medical vested interests protect the HIV/AIDS paradigm. The government-controlled peer review grant system is a key tool for protecting paradigms like this.

Bauer (2004) proposes that there be mandatory funding of contrarian research, along with a science court set up to adjudicate technical controversies. In addition, science journalism needs to investigate established orthodoxies more vigorously.

Pollack (2005) proposes several remedies to the competitive peer review grant system. Government should establish forums where the most significant challenge paradigms can compete openly with their orthodox counterparts in civilized debate. Open-minded "generalists" who have no stake in the outcome should adjudicate, like a jury does in law. Pools of money should be set aside to support multiple grants on selected schools of thought. Training grants that encourage curiosity and thinking outside the box should be made available. And the NIH should provide lifetime support for a select cohort of Dionysian scientists.

The peer review grant system stifles innovation and protects reigning paradigms, right or wrong. The 60-year experiment of "Advancing Health through Peer Review," the NIH Center for Scientific Review’s slogan, has failed. It needs to be dismantled. Tax-funded research would be better conducted and more productive if government allocated funds directly to universities and foundations to use as they see fit for advancement of the biomedical and physical sciences.

One alternative to the competitive peer review grant system that the NIH and NSF might consider for funding specific research projects is DARPA, the Defense Advance Research Projects Agency. This agency manages and directs selected research for the Department of Defense. At least up until now it has been "an entrepreneurial technical organization unfettered by tradition or conventional thinking" within one of the world’s most entrenched bureaucracies (Van Atta et al., 2003). Eighty project managers, who each handles $10-50 million, are given free reign to foster advanced technologies and systems that create "revolutionary" advantages for the U.S. military. Managers, not subject to peer review or top-down management, provide grants to investigators who they think can challenge existing approaches to fighting wars. So long as the state controls funding for research, managers like this might help break the logjam of innovation in the biomedical and physical sciences.

Science under the government grant system has failed and new kinds of funding, with less government control, are sorely needed.

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This paper, titled "The Government Grant System: Inhibitor of Truth and Innovation?", was published in the Spring 2007 issue of the Journal of Information Ethics 2007;16:59-69.

**Donald Miller is a cardiac surgeon and Professor of Surgery at the University of Washington in Seattle.

==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?

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.

http://www.duesberg.com/papers/chemical-bases.html

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).

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