BENEATH RUGGIERO'S RAINBOW
FABIO FRANCHI
Translation by TIG: www.tig.org.za
Over the past few years, Professor Marco Ruggiero has featured in a remarkable number of scientific research studies, proposals and initiatives that have taken him to the heights of the scientific world – or, at least, of the rainbow, as Celia Farber has it in her interview with him in October (here). An admirable achievement!
But what’s the reality behind the appearance? I’ve remained silent until now, so as not to throw a wet blanket on his dazzlingly original research. But it’s high time everyone found out how he’s gone about things, because I think it’s been tremendously counterproductive to our pursuit of the truth about so-called HIV/AIDS.
For anyone with the patience to read, I’ll describe the origins of Ruggiero’s work with GcMAF and how he cut me out of it. For actually it was I who introduced him to the ideas and proposals that he promptly made his own in his research. This is set out in Part 1. In Part 2 I’ll describe some technical and theoretical defects in his recent research output, revealing the confusion and imprecision that characterizes his writing and his claims, and I’ll show that some of his claims are lies. His statements concerning HIV/AIDS are addressed in Part 3.
These sections stand independently of each other.
PART 1. PROFESSOR RUGGIERO AND GCMAF
It’s a long story, but I’ll try keeping it short and will highlight just the main details so as to indicate his ethical character.
I first contacted the professor from Florence at the beginning of 2009 (I already knew of him because he's also an AIDS dissident) to propose a collaboration with Dr Yamamoto to finally ascertain whether his claimed successes in the treatment of cancer and AIDS were true, even partly so. I’d previously found and demonstrated several inconsistencies in Yamamoto’s papers by way of a dedicated investigative analysis that turned up many surprises.
Since Yamamoto had failed to answer the many questions I’d asked him, I discovered these irregularities after writing to the editors of the journal that had published his research, with the result that he got a bit annoyed with me. I conveyed these data to Ruggiero, because he was placed to perform the appropriate tests and checks in his laboratory. Ruggiero agreed to contact Yamamoto to suggest a collaboration, although more as a favour to me than out of conviction. Yamamoto agreed in turn, but claimed to be temporarily out of GcMAF stock and was preparing more, and so wanted to postpone the collaboration for several months.
Ruggiero and I were sceptical, so I repeatedly urged him to write to Yamamoto again. Ruggiero was convinced that Yamamoto was going to put us off indefinitely and I wanted to keep the pressure up.
At the end of December 2009 we were surprised when Ruggiero received a parcel from Philadelphia, where Yamamoto has his Socrates Institute. Ruggiero was curious but at the same time regretted having committed himself, and said: “I’ll test the GcMAF he sent you right away but it will probably be a waste of time, and we’ll soon be able to focus on more important things.”
A few days later things changed. Ruggiero told me excitedly that his initial tests were a great success and had produced the expected results, adding, “I think I’ll redirect great part of my research on GcMAF.”
Ruggiero and I exchanged some emails and I travelled to Florence twice to meet him. He was increasingly excited and so was I.
He told me he’d presented six abstracts to the Vienna conference, and that the only one accepted was that in collaboration with Yamamoto.
The next thing was he said he couldn’t exchange any information with anyone because he was being spied on and wiretapped. Claiming his research could be blocked, Ruggiero discontinued almost all contact with me (notwithstanding that I’d acquired a dedicated telephone especially for our exchanges). Ruggiero told me we could resume contact again in July 2010 after the Vienna conference.
In the meantime, and without regard for the danger that he'd alleged to me, Ruggiero prominently posted his collaboration with Yamamoto on his website, thereby telling the world what he said he could not tell me (he told similar things to people who wrote to him privately).
Just before this development, I’d naively suggested to him that thanks to his good relationship with Yamamoto I might also participate in the research collaboration (one might have expected him to have proposed this of his own accord). He never replied. Yamamoto himself had agreed.[1]
Ruggiero’s research with Yamamoto turned out to be a huge success for him and was followed by a great stir in the media, publications and funding.
But did he remember me? Sure he did! Even though he could no longer spare the time to email or phone me, he very considerately stated in an interview with Piscitelli on 13th October 2010 in Il Predellino (!): “In Italy, one of the first people to recognize the potential of these results was a specialist in infectious diseases, Dr Fabio Franchi of Trieste, who tried to alert people potentially interested in this and contacted several researchers, both Italian and foreign, hoping to apply Yamamoto’s observations to the development of new therapies.” And that was it.
Most people will consider the scientific issues more important than Ruggiero’s ethical conduct, so I’ll focus on the former.
Ruggiero wrote: “Since these are preliminary clinical experiments approved by Nagasaki and Hyogo Universities in Japan (the documents are available), the number of patients was limited, about ten, but the results were nonetheless striking. These results were unreservedly accepted by the international scientific community thanks to the peer review system.”
How does one describe cases like these? Ruggiero lies and he knows he’s lying because I gave him the data contradicting his claims. In fact, Nagasaki and Hyogo Universities did not approve anything at all and the ethics committees that allegedly approved Yamamoto’s research are invalid, utterly invalid: they’re disqualified, because several of their members, including the two chairmen, are co-authors of some of his papers,[2] a self evident conflict of interest. Furthermore, the documents (questionnaires, the informed consent form) were written in English only in June 2009 (the file properties show this!). This means, logically, that the African patients of South Africa, those of South Asia and the sole lost American patient were supposed to read the questionnaire in Japanese at the time they were recruited. He did not know who the patients were, nor did the members of the committees.
The peer reviews of Yamamoto’s papers were only formal, as I have comprehensively demonstrated. There were no data controls, yet they were accepted without a murmur.[3]
But there’s more about Ruggiero, both as a man and as a scientist. The following are some observations about his claims.
Part 2. TECHNICAL OBSERVATIONS CONCERNING PROFESSOR RUGGIERO’S PRESENTATION
(See http://j.mp/fBZx9K)
According to Ruggiero, referring to HIV+ patients treated by Yamamoto with GcMAF (Slide 37), “The people treated are real and some of them well known by Yamamoto.”
It’s strange that Yamamoto had difficulty finding the only patient in the USA and was ultimately unable to do so, as he stated when asked by the editors of the journal in which his paper had been published.[4] The question is: did Ruggiero actually meet any of them himself? It’s hard to say, because the patients described by Yamamoto (with the above exception) are scattered throughout South East Asia and South Africa:[5] So how did he manage to perform all the tests described in his papers? In other words, how did he manage to get different laboratories in different countries to have exactly the same standards and procedures?
The following point is very important and it’s very odd that Ruggiero missed it, because he frequently expatiates on the specificity and the sensitivity of the diagnostic tests (Slide 40): I was unable to find any validation of the nagalase levels determination in comparison with other cancer markers, and with “HIV” viral load (for present purposes, let us allow for a moment that “viral load” is a real reference). Any test should be validated before presenting it. This test is part of Yamamoto’s model and is used as a follow up tool for the treatment. The comparison between nagalase level, viral load, p24 and plaques (to quantify “free virus” and “infected cells”) specified in the charts of J Med Virol 2009;81:16-26, shows a nearly perfect correlation. The same can be said for the correlations between nagalase and tumour markers in Yamamoto’s papers published in 2008. The “viral load” has been compared by the Japanese researcher to a particular test involving “centres of infectivity” in cell cultures (also incidentally “infected” with HTLV-I), capable of distinguishing “free viral particles” from “infected” lymphocytes. But where are the studies that show, with appropriate controls, those perfect correlations? These results certainly are strange because everybody knows, for instance, that no correlation exists between “viral load” and number of “infected” cells and/or p24 level. Today, nobody uses this plaque assay notwithstanding its allegedly unique capability, according to some researchers, to distinguish “pathogenic” from “non-pathogenic HIV”![6]
Moreover, such a fine correlation hasn't been confirmed properly by the disappointing results in other independent studies.[7]
Slide 50: Ruggiero supports Yamamoto’s claims about eradicating “HIV”. But isn’t Ruggiero perfectly aware that “HIV” has never been isolated and proved to exist?[8] Evidently, he likes to support radically different, contradictory scientific positions simultaneously. This hardly reconciles with his claimed rigorous and logical approach to science.
In fact, Ruggiero’s claims are fraught with considerable theoretical difficulty. As I’ve already commented concerning Montagnier’s “unconventional” recent statements, all retrovirologists claim that ”HIV” inserts itself into cellular DNA and so can only be eliminated by killing all infected cells, which cannot be distinguished for this purpose from uninfected ones. Even Dr Andrea Savarino, with his shock and kill treatment approach, recognizes the problem.[9] This view is accepted by all retrovirologists, both dissident and non-dissident, other than Montagnier (only sometimes) and Yamamoto. The thinking is: “Once infected, always infected” (the same notion has been repeated by Ruggiero himself in another context).[10] Needless to say, as Papadopulos-Eleopulos observes, it’s pointless attempting to eliminate a non-existent virus.
By supporting Yamamoto, however, Ruggiero endorses the existence of ”HIV” and the need to get rid of it by “strengthening”, that is, stimulating, the immune system. He endorses Yamamoto’s claims to have eliminated it in several subjects. He claims he’s confirmed that Yamamoto’s patients really exist, and I hope it's true, because I’m going to follow up on this. Some time ago, claiming privacy issues, Yamamoto refused to put me in contact with these patients and/or their doctors.
There's another problem to solve, both theoretical and practical: In AIDS there’s often (if not always) chronic immune activation, which is partly controlled and reduced by “antiretroviral” therapies and by appropriate antioxidant treatment. Since GcMAF is active, can it have a beneficial regulating effect or does it run the risk of exacerbating the problem? I repeat once again: What is found in vitro cannot simply be extrapolated, because in vivo the stimuli and inhibition systems are much more complicated. For instance, according to some researchers like Andrea Mantovani, there are allegedly several types of macrophages, one of which combats tumours and another stimulates their growth.[11] This is why there are many stages in drug research, and no one stage guarantees the success of the next.
Slide 67 tells us: [Ruggiero’s own translation]: These results can prove instrumental in identifying those subjects that could benefit the most from GcMAF treatment, in particular considering that such a treatment is currently being proposed in different settings (see for example: http://j.mp/gL4lOx and http://j.mp/eiwUlS)
This explains some unaccounted facts. I don’t think Ruggiero is advising people not to turn to order the non-original GcMAF from internet sites. On the contrary!
But why do I raise this point? Because, reviewing the history, we find three different phases (see footnote[12]). I include it in a note because it concerns an “unethical” behaviour to my detriment, not a scientific issue.
PART 3. RUGGIERO’S SCIENTIFIC APPROACH AS AN AIDS “DISSIDENT”
Ruggiero’s approach is harmful because it piles confusion upon confusion. As I’ve mentioned before, his style in propounding diametrically contradictory positions make hard to understand the real issue. Ruggiero is simultaneously Duesberg’s supporter (“HIV is not the cause of AIDS” which means “HIV is a harmless virus”); Montagnier’s and Yamamoto’s (“HIV is a pathogenic virus”, that is, “HIV is not the sole cause of AIDS”, which means: “HIV is one of the causes of AIDS”); a staunch supporter of Papadopulos-Eleopulos (except that so far it seems he has not understood what she’s saying); as well as a staunch supporter [13] of de Harven’s view (“Montagnier found a retrovirus, but it’s not HIV”, see the Perth Group’s analysis[14]). How can all these positions be consistent and reconciled at the same time? How can they be understood by other researchers, lay people and HIV+ persons?
The note[15] contains a critique of a paper of his.
CONCLUSIONS
What can I say? It’s the way of the world. Surely the important thing is to verify the real effects of Yamamoto’s treatment in HIV+ or cancer patients. The rest is secondary. But I find curious and inexplicable the behaviour of this scientist, who says things that are simply not true. This is no way to pursue scientific truth. Ruggiero makes it difficult to trust anything he claims.
In my view, Ruggiero’s scientific claims threaten to compromise and reverse the serious work of those scientists, who, unlike him, have forsaken honours and lucrative careers in their absolute and uncompromising fidelity to scientific truth.
APPENDIX
1. The following is Ruggiero’s endorsement of Yamamoto’s claims, which implicitly include his acceptance of the existence of “HIV”:
“Our results are consistent with those of Prof. Yamamoto who demonstrated that GcMAF treatment leads to eradication of HIV in seropositive patients”. [Ruggiero’s own translation]
Celia Farber asked Ruggiero (in his “rainbow” interview): “Do you think HIV exists as a unique and exogenous retrovirus?” Ruggiero answered: “Yes, I do”.
2. What were the true results?
In Cancer Immunol Immunother, Pacini et al. (online on 14 December 2010) published a paper where Ruggiero described their research with the original GcMAF sample from Yamamoto and another two samples from England (in fact I’d sent them to him). I asked Ruggiero to check them for activity and cell toxicity, and he did so. After several reminders, Ruggiero finally sent me an anonymous file. He made sure not to send me all the data! Only, by reading the published research I realized that some of the data he had given me were radically different from the published data.
[1] Yamamoto wrote to me on 21 July 2009: “I am also pleased that you made an arrangement for study of GcMAF therapy of Erlich ascites tumor in BALB/c mice with the University of Flore.”
[2] I found that four members of the two committees (Nakazato H, Koga Y, Suyama H and Urade M), including the two IRBs chairmen, were co-authors of Dr. Nobuto Yamamoto's several papers on nagalase and/or treatment with GcMAF.
The chairmen of those committees don’t even know where the patients are and by whom they have been “treated” (Dr. H Suyama wrote: “We believe that every patient is treated by own physicians and not in recognizable hospitals.”)
One member of the Japanese Ministry of Health told me: “My friend who is a professor (Immunology) and Dean of the Nagasaki University did not know the presence of such Committee in Nagasaki.”
The ethics committees were not registered as such. Regarding this, H. Suyama (IRBs chairman) admitted: “they may not recognize us and we must register again.”
The IRBs questionnaire was generic and completely inadequate for the correct information of the patients (I can send it upon request).
[3] The editors of the J Med Virol themselves (pressed by me) wrote to experts around the world to enquire about the ethics committees and the patients. They asked others what I asked them. There is no question that these data were not checked by the “double peer review” before publication.
The patients were as follows: one in the USA but lost at follow-up 10 years ago; the remaining ones, according to Yamamoto, were scattered in South East Asia and in one or more South African Countries.
[4] The only American patient. Yamamoto wrote on 21 July 2009: ”At the present we are in the process of locating an American patient who was treated in the late 1990s. As you can imagine, such follow up after a decade is not a simple matter.” Was the follow-up of the South African patients any easier?
[5] African patients. The chairman Dr H. Suyama wrote to the editor of J Med Virol: “Physicians from Southeast Asia and African countries requested for supply of GcMAF for treatment of HIV patients and patients are living in various locations in those countries.”
[6] Plaques distinguish pathogenic “HIV strains”: “[…] The plaque-forming HIV all came from patients with disease; no healthy seropositive individuals had these types of isolates. Plaque formation may be a useful assay for identifying pathogenic strains of HIV.” Tateno M, Levy JA. MT-4 plaque formation can distinguish cytopathic subtypes of the human immunodeficiency virus (HIV). Virology. 1988 Nov;167(1):299-301.
[7] No good independent results:
a) Rehder DS, Nelson RW, Borges CR. Glycosylation status of vitamin D binding protein in cancer patients. Protein Science, 2009 Jul 29.
Abstract: Based on the results of activity studies, previous reports have suggested that Vitamin D Binding Protein (DBP) is significantly or even completely deglycosylated in cancer patients-eliminating the molecular precursor of the immunologically important Gc macrophage activating factor (GcMAF), a glycosidase-derived product of DBP. The purpose of this investigation was to directly determine the relative degree of O-linked trisaccharide glycosylation of serum-derived DBP in human breast, colorectal, pancreatic, and prostate cancer patients. Results obtained by electrospray ionization-based mass spectrometric immunoassay showed that there was no significant depletion of DBP trisaccharide glycosylation in the 56 cancer patients examined relative to healthy controls. These results suggest that alternative hypotheses regarding the molecular and/or structural origins of GcMAF must be considered to explain the relative inability of cancer patient serum to activate macrophages.
b) Marilena Greco et al. Serum proteomic profile of cutaneous malignant melanoma and relation to cancer progression: Association to tumor derived alpha-N-acetylgalactosaminidase activity. Cancer Lett. 2009 Apr 24.
(I talked to the lead author who confirmed the poor correlation between tumour and nagalase level and Ruggiero was informed about it.)
[8] Ruggiero acknowledges the Perth Group's science, which is quoted extensively in his student JJV Branca's thesis which he supervised: http://j.mp/hSwYBo.
[9] Savarino's 'Shock And Kill' Research Gives New Hope For HIV-1 Eradication, see http://j.mp/dOVAFh.
[10] See note 8.
[11] Mantovani A et al. Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes. Trends in Immunology. 2002 Nov;23(11):549-555
[12] THE THREE DIFFERENT PHASES OF RUGGIERO’S ATTITUDES TOWARDS THE “NON-ORIGINAL” GCMAF
Ruggiero’s initial behaviour was open; he did not actually discourage me from carrying out my own research – which I shared with him – and which involved my testing the substance from England before others. He also freely encouraged other seropositives (I have clear written and verbal evidence of this).
Then came the intermediate phase in which, without informing me before or afterwards, Ruggiero privately warned people against reading about GcMAF on the Internet, obtaining it and trying it other than in clinical trials (thus creating special difficulties for me). And at the time that he was asking me to keep his research private and to discontinue our communications, he wrote to an HIV+ person (I quote verbatim): “As a doctor, I advise you strongly, earnestly, absolutely, not to be persuaded by anyone to try out any sort of treatment for any kind of disease that is not administered in an approved clinical trial, controlled by the authorities in charge and that can be objectively monitored.” Ruggiero pertinently avoided asking Yamamoto for some GcMAF for me (both for so-called compassionate treatments in appropriate cases and for well-defined clinical research). He could easily have done so and Yamamoto would readily have agreed.
The third phase came about when he seemed to reverse his aversion to websites offering GcMAF with a slide that I understand is an invitation to consider what they’re offering. His change of heart is unexplained.
I don’t know and I’m not interested in knowing his current phase.
[15] Ruggiero’s poster publication, “HIV and apoptosis of cancer cells: the killer’s promises” at the Annual Conference of the Italian Association of Cell Cultures in December 2009 is even more amazing: He indirectly assists the opponents of the AIDS dissidents, making it easy for these opponents to refute their arguments.
In the poster Ruggiero wrote: “In the past three years definitive evidence has accumulated demonstrating that HIV is not the (sole) cause of AIDS.” What this means is that HIV exists and is one of the causes of AIDS. The parentheses he inserts are meaningless.
Then he becomes more explicit: “Clearly HIV cannot be the cause of AIDS” because it “has been present in humans since at least the early 1900s.” This is taken as a given in the article he cites, and the method used for this great discovery is the PCR (epidemiology based on molecular beacons), that is said to be undoubtedly specific, but is it? Ruggiero has contradicted this on several occasions in stating that it was not so specific and the virus has not been “properly” isolated. Ruggiero lends support to the authors who allege an HIV epidemic, albeit only with a limited number of clades. Then, according to the data Ruggiero provides to the reader, the correlation is evident between AIDS and HIV. Ruggiero now says: “The very fact that AIDS was never described before the 1980s proves that it is not the cause.” Duesberg long ago showed that AIDS-related diseases were well known in the past but not recognized as AIDS. It is understandable: If there were a few, isolated cases, they could well have remained unnoticed before AIDS appeared as an epidemic in the 1980s, which in turn can be properly correlated at this point with the spread of the “clades”. In short: a red carpet for the “orthodoxy”!
In his poster, Ruggiero also proposes a symbiotic (advantageous) association between HIV and humans, forgetting that a few lines above he claims, as Montagnier does, that “immunodeficiency causes chronic HIV infection”. In so doing, he unwittingly affirms the pathogenicity of HIV, claiming that a chronic viral (and HIV) infection can change from innocuous to extremely dangerous in immunodeficient states. Consider for example CMV infection. An advantage (or a symbiosis) most people would prefer to spare themselves.
Moreover, immunodeficiency cannot cause infection; it is independent. According to retrovirologists, HIV infection once caught is always chronic by its (purported) nature.
Regarding “HIV” and cancer, Ruggiero could say that a particular protein is anti-carcinogenic, but before saying that it comes from “HIV”, one might ask him where is the proof of it, as the Perth Group has done (did he read the Perth Group properly, or didn’t he?).
Ruggiero maintains that “epidemiological data show that HIV is not permissive of breast cancer”, and he cites for that a paper counting 64 cases of breast cancer (in the literature) in HIV positive African women (J Women’s Health 2003;12:227-32) in which the authors mention “the paucity of available data”. Anyway, even with those modest data, it seems that this protection is, at best, only a modest one!
Strange enough, the Vpr found in HIV patients is anti-inflammatory. Strange enough, because seropositive patients with diminished immune function are characterized by a chronic inflammatory state.
Conclusion: Ruggiero may think he’s found the magic bullet to kill cancer cells, but without a doubt he’s found the magic bullet to shoot also his “dissident science”!