I’ll Have the Mayo, Hold the Reuben

The academic blogosphere is buzzing with the recent discovery of a major incident of academic fraud.  Dr. Scott Reuben published 21 papers over the course of 12 years that have been implicated in the fraud, making this one of the largest cases of academic fraud ever discovered.  Worse yet, Dr. Reuben’s research is in medicine, throwing a primary method of post-surgical treatment into disarray.

The Good

Not everything about this story is bad.  First, the fraud was discovered because science is self-correcting.  This feature is what makes science such a powerful tool.  Specifically, Dr. Reuben had recently submitted two study abstracts, but the internal reviewer at his medical center discovered that he had failed to obtain approval to do human research for those studies from the IRB.  Any research on human subjects is required to receive approval from the sponsoring institution’s IRB, detailing the exact protocols and experiments to be performed in order to make sure that any such research is ethical.  Even altering a questionnaire can result in significant penalties.  The internal reviewer noted discrepancies and irregularites in some of Dr. Reuben’s other papers, triggering a full scale review.  Another positive is that Pfizer, the pharmaceutical company that produces the medicines implicated by this scandal and has funded at least some of the research, has announced that they will be releasing an annual list of doctors to whom they have funded more than $500 the previous year.  Although the monitoring period will not begin until July 1st of this year, it creates a more transparent system so that potential conflicts of interest are more readily apparent.  Finally, due to the sweeping nature of the fraud, this may be the tipping point in getting a central database of ongoing medical studies.  This database would permit tracking of medical studies so that negative and inconclusive studies don’t get buried by publisher bias towards positive studies.

The Bad

The research now believed to be fraudulent established the primary protocol for administering non-narcotic analgesia for certain surgeries.  In layman’s terms, these studies are how we determine what painkillers and their doses following surgery, without using opiates like morphine.  Although the existing protocols are safe, new studies will have to be commissioned in order to find out whether the protocols are effective and if they need to be altered.  In the meantime, other methods, once thought to be less safe or less effective, will have to be used.  This sets us back several years, at best.  This is devastating news.

The Ugly

Even worse, it is likely that several pseudo-science groups will attempt to use this fraud to promote their agenda.  What makes this particularly galling is that pseudo-science is endemic with fraud, yet they will rally around the fraudulent researcher and defend him against all evidence.  A recent example of this behavior is the response to the revelation that Andrew Wakefield’s paper implicating vaccines in autism was based on fraudulent data.  Compare the responses:

  1. Dr. Reuben: scientists immediately withdraw the offending papers, discard the results, and immediately look for ways to uncover fraud earlier
  2. Dr. Wakefield: pseudo-scientists immediately attack the person who discovered the fraud, circulate a petition supporting Wakefield, and try to cover up the fraud

Another ugly aspect, independent of concerns about pseudo-science, is that this undermines public trust in medicine and the government.  Many people will assume that the medications are unsafe, even in other applications that are not implicated.  Funding for science and medicine is jeopardized as well.


3 Responses to “I’ll Have the Mayo, Hold the Reuben”

  1. Michael Says:


    No need to publish this. It is simply fyi:

    I noticed that you had posted on aetiology that the pix presented there as being hiv are somehow proof of hiv.

    Not good enough, my friend, any more than that pix of ufo’s are real.

    None of the hiv pix verify that any such thing in the picture is actually of a “HUMAN IMMUNODEFICIENCY VIRUS”. There is no proof with any of those pix that what was photographed was actually an exogenous retrovirus that somehow, mysteriously, causes immune suppression.

    In the words of expert electron microscopist and aids “denialist” Etienne de Harven:

    In the case of RNA tumor viruses, now called retroviruses, the demonstration of viremia in the blood plasma of experimental leukemic animals (chickens and mice) was published more than 35 years ago. A most efficient purification method including ultrafiltration and ultracentrifugation of a 1/1 dilution of plasma in heparinized Ringer’s solution, allowed me to demonstrate packed retroviruses by transmission electron microscopy (7) in thin sections of pellets obtained by high speed centrifugation of the purified virus, quite clearly establishing that the amount of contaminating cell debris was remarkably small, a conclusion which could never have been reached by using the negative staining EM method. Using this simple ultrafiltration procedure, virions were never exposed to hypertonic shock. However, sedimentation in sucrose density gradients, at the density of 1.16 gm/ml, soon became the most popular method for retrovirus purification.(8) Interestingly, it was very well known by electron microscopists in the 1960s, that sharp bands sedimenting at the density of 1.16 frequently contained large amounts of microvesicles and cell debris of non-viral nature. These debris just happened to sediment in sucrose gradients at a density very similar to that of retroviruses clearly indicating that finding a “sharp band” at the density of 1.16 gm/ml was of little significance and was certainly far from any demonstration of retroviruses isolation.

    But this conclusion was based on EM findings, and around 1970 the faith in retroviral oncology was assuming quasi-religious proportions! If EM cannot demonstrate viruses in the 1.16 bands, let us forget about EM and rely on other “markers”!

    When around 1980, R. Gallo and his followers attempted to demonstrate that certain retroviruses can be suspected of representing; human pathogens, to the best of my bibliographical recollection, electron microscopy was never used to demonstrate directly viremia in the studied patients. Why? Most probably, EM results were negative and swiftly ignored! But over-enthusiastic retrovirologists continued to rely on the identification of so-called “viral markers”, attempting to salvage their hypothesis.

    When retrovirus particles are legion, the study of molecular markers can be useful, and provide an approach to quantification probably better than direct particle counting under the EM (which I always found very difficult). But when, using EM, retrovirus particles are absent relying exclusively on ‘markers’ is a methodological nonsense. ‘Markers’ of what?

    Nevertheless, for the past ten years, HIV research and clinical therapeutic trials have been primarily based on the study of several HIV “markers”.

    First the antibody. Elisa, then Western Blot tests were hastily developed (at sizable financial profit eagerly split between the Pasteur Institute and the US). “Seropositivity” became synonymous with the disease itself, plunging an entire generation into behavioral panic, and exposing hundreds of thousands of people to ‘preventive’ antiviral AZT therapy which actually hastened the appearance of severe or lethal immunodeficiency syndrome. Appropriate controls were apparently never carried out or were never published. Still, back in 1993 it became clear that the so-called HIV antibody tests badly lacked specificity, (9) cross-reactivity being observed with patients suffering from a long list of pathological conditions including malaria, leprosy, auto-immune diseases and many more.

    Secondly, ‘viral proteins’. Several proteins have been identified as ‘HIV markers’, most frequently because they were identified in a variety of 1.16 bands. The case of the p24 “viral” antigen is a significant example and its lack of viral specificity has been well documented.(10)

    Third, reverse transcription. If reverse transcriptase activity were a unique feature of retroviruses, it could have been an interesting molecular marker. Unfortunately, it has been shown that reverse transcriptase is found in the uninfected cells of yeasts, insects and mammals (11) and “has nothing to do with retroviruses as such” as well referenced in a recent report from S. Lanka. Moreover, K. Mullis himself does not support the use – to amplify and quantify the “HIV genome” – which is being made of the PCR methodology he developed, which is the current method of “measuring the viral load” in AIDS patients.

    More disturbing is the fact that some ‘markers’ are searched for in the 1.16 gradient sedimenting material which is the density where intact virions are expected to be found, but not their molecular fragments. If lysed retrovirus particles released molecular markers, the 1.16 samples should at least initially allow investigators to demonstrate virus particles by EM. They don’t. however after 15 years of most intensive HIV research, two independent groups finally decided to explore by electron microscopy the ultrastructural features of the material sedimenting at the 1.16 density. Working on “HIV-1 infected T-cell” cultures supernatants, both groups found that it contains primarily cellular debris and cell membrane vesicles which could definitely not be identified with HIV particles and rare “virus-like” particles.(12, 13) Still, this is the type of sample in which “viral markers” are currently identified and used to measure the effects of anti-viral drugs in current clinical trials.

    In conclusion, and after extensive reviewing of the current AIDS research literature, the following statement appears inescapable: neither electron microscopy nor molecular markers have so far permitted a scientifically sound demonstration of retrovirus isolation directly from AIDS patients. This conclusion fully confiens the recent reports published in Continuum by E. Papadopulos and by S. Lanka.

    Harvey Bialy, editor of the journal Bio/Technology has stated that (14) “A powerful hypothesis has to explain and predict. What kind of scientist continues to support a hypothesis that fails to explain and fails to predict?” The HIV/AIDS hypothesis fails to explain the considerable drop of T4 circulating lymphocytes in AIDS patients. It predicted a dramatic AIDS epidemic which was never observed (unless we accent the CDC’s most surprising redefinition of AIDS as including some 31 “AIDS defining illnesses”!).

    Obviously, the HIV/AIDS hypothesis has to be scientifically reappraised.(15) And, most urgently, the funding for AIDS research should no longer be restricted to laboratories working on an hypothesis which has never been proven. *

  2. Michael Says:

    As for Etienne de Harven’s creds? They are impeccable:

    Dr. Etienne de Harven is emeritus Professor of Pathology, University of Toronto. He worked in electron microscopy (EM) primarily on the ultrastructure of retroviruses throughout his professional career of 25 years at the Sloan Kettering Institute in New York and 13 years at the University of Toronto. In 1956 he was the first to report on the EM of the Friend virus in murine (mouse) leukemia, and in 1960, to coin the word “budding” to describe steps of virus assembly on cell surfaces.

    And by the way, regarding the original so called “isolation” of hiv, then known as LAV, here is Etienne’s quite recent letter to the Nobel Prize committee:

    The Nobel Prize for Barré–Sinoussi and Montagnier
    The Nobel Prize in medicine has been recently awarded to Barre-Sinoussi and Montagnier for “The discovery of immunodeficiency virus (HIV)».
    This award is, to a large extent, based on a paper published by the laureates et al. in May 1983, in «Science» (vol 220, pp 868-871). The conclusions presented in this paper result, in a large part, from observations made by transmission electron microscopy. Having been responsible for research on electron microscopy of retroviruses, at the Sloan Kettering Institute of New York from 1956 until 1981, I do have scientific competence to raise the following questions related to the significance of the paper under reference.

    This 1983 paper is illustrated (Fig. 2) by an electron microscopy image of thin sections of virus-producing cord lymphocytes. Three day old cultures of T lymphocytes from two umbilical cords had been «infected with the cell-free supernatant of the infected coculture». This «coculture» consisted of cultured human normal T lymphocytes admixed with lymphocytes that originated from the lymph node biopsy from one patient «at risk for acquired immune deficiency (AIDS)». The author’s interpretation of Fig.2 is that it demontrates that cord blood lymphocytes had been successfully infected by retroviruses from that patient.

    Unquestionably, Fig 2 illustrates typical retroviruses (C-type), budding from the surface of a lymphocyte.

    Highly questionable, however, is the origin of these retroviruses.

    The authors of the report claim that they originate from the patient lymph node, via the «cell-free supernatant» of the coculture.

    This interpretation is not satisfactorily supported by the data presented.

    Indeed, if this interpretation was correct, one would have expected :

    1) evidence, by electron microscopy, of the multiplication of retroviruses in this «coculture», and
    2) evidence, again by electron microscopy, for the presence of retroviral particles in the «cell-free supernatant of the infected coculture».

    Since 1) and 2) evidences are totally missing, how could the authors of this paper justify their claim for having «infected» the cord lymphocytes with the «cell-free supernatant of the coculture» ?

    The authors have regarded their «coculture» as «infected» only on the basis of reverse transcriptase activity in sucrose fractions from the supernatant. Sucrose fractions at density around 1.16, however, are known to contain large amounts of cell debris that can readily account for the observed transcriptase activity. In short, one is asked to believe that cord blood lymphocytes have been sucessfully infected with the supernatant of a coculture the viral infection of which has not been demonstrated.

    As indicated above, Fig. 2 of the paper shows typical retroviruses (C-type) budding from the surface of a lymphocyte. Where are they coming from, if it is not from the «cell-free supernatant of the coculture» ?

    There is another possible explanation for the viral electron microscopy evidence of Fig. 2, an explanation that did not, obviously, received the slightest attention from Barre-Sinoussi, Montagnier et al.

    The observed cultured lymphocytes came from cord blood, and therefore originate from the placenta. It is well known, since the late 1970’s (Sandra Panem’s work, in Current Top Pathol, 1979, 66 :175-189), that the normal human placenta contains loads of C type retroviruses (HERVs). Placental lymphocytes are, therefore, likely to contain the same HERVs that, when placed under stimulating culture conditions, may bud from cell surfaces and form complete retroviral particles (C-type) recognizable with the electron microscope (Fig. 2). Barre-Sinoussi et al. avoided to explain why their experiment apparently wouldn’t work with lymphocytes from the peripheral blood, instead of those from cord blood? The simple explanation is that human peripheral blood lymphocytes do not harbor HERVs.

    In my opinion, Fig. 2 illustrating the paper under consideration totally fails to convincingly demonstrate that the observed retroviruses originated in the lymph node of one patient «at risk of acquired immunodeficiency syndrome». There is no scientific reason, therefore, to refer to these particles as «LAV» nor as «HIV». Referring to these particles as «LAV» or «HIV» mislead the Nobel Committee, and resulted in a seriously questionable award of the Nobel prize.

    Etienne de Harven, MD, Emerit. Prof, Univ. of Toronto.

  3. W. Kevin Vicklund Says:

    I noticed that you had posted on aetiology that the pix presented there as being hiv are somehow proof of hiv.

    No, I didn’t. Cooler claimed that no EM’s existed (and kept changing the criteria). All I did was point out that an EM matching his criteria did exist and that it supported the HIV->AIDS claim. By itself, a single EM proves nothing – and frankly, science demonstrates, not proves. But in combination with lots of other data, it is reasonable to accept that the EM is what it is claimed to be – not even cooler denied that it was HIV.

    What I posted was extremely modest in its intended scope – that there existed EMs which cooler claimed didn’t exist. It was a claim that even a non-expert like myself could easily demonstrate to be false.

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