What is a "scientific fact"? A small case study: The "measles process"

by Professor Harald Walach

Publication date of the article unknown

A single study, even if well published, does not constitute a fact. The data must also be replicable, preferably independently, preferably by other groups using the same or a similar method. Is that already enough?

No. Because science is a social process. And an essential part of what is scientifically accepted depends on the consensus of a community of researchers and specialists. Ludwik Fleck was the first and very prominent to point this out in the 1930s. He showed how difficult it actually is to determine what a syphilis spirochetes is, i.e. the bacterial pathogen that causes syphilis. With this example he was able to demonstrate how crucial social processes are in scientific consensus building.

One can summarize his position in the bon mot: "A scientific fact is the agreement to stop thinking".

I will illustrate this in the following with an exciting current example: using the "measles virus process" and the question "Does the measles virus really exist?

Initial situation

In the so-called "measles virus trial" the question is whether Dr. Stefan Lanka owes Dr. Bardens the prize money of 100,000 euros. This will be paid out "if a scientific publication is presented in which the existence of the measles virus is not only claimed but also proven and in which, among other things, its diameter is determined. [1] Dr. Bardens has presented six studies that he believes meet the criteria. Dr. Lanka has denied this. Dr. Bardens won the prize money in a civil lawsuit. The defendant, Dr. Lanka, has filed an appeal.

This is a highly interesting situation: an individual who is competent in the matter denies the consensus of the majority. He does this with the help of a provocation in the form of prize money; otherwise probably no one would care about this provocation. We can already consider at this point: how useful is this call for entries - beyond the intended provocation - at all? Is it even possible in principle to want to prove any fact with a study? I can abbreviate for impatient readers: In my opinion, this is not possible in principle. Nowhere. Not in any field. The measles virus process is a good example to illustrate this.

The question that needs to be answered is therefore whether the work presented - see below for details - is scientific and suitable for the detection of a measles virus. I have taken a look at the six papers because I find this discussion exciting and would like to express a few thoughts on it.

This also addresses what it is not about and what (to avoid misunderstandings) is not the subject of this article:

• It is not about clarifying whether measles exists or not. It goes without saying that measles exists as a clinical-pathological entity.
• It is also not about clarifying whether measles is caused by any virus or not,
• and certainly not whether measles vaccination is effective and sensible.

What does "scientific" mean in this context?

The concept of scientificity

Scientificity is a complex construct. The fact that a text has been published in a scientific journal says no more and no less than that competent readers and colleagues understand the text, have found it to be correct and good, and that editors and reviewers of the journal find the text interesting for their readership, usually a specialist audience. It does not say anything about the truth content or the quality of the information published there. In this sense, all but one - see later - of the publications presented in this process are "scientific". They meet the minimum standard of having been published in a scientific organ.

However, the concept of scientificity also includes consensual, social acceptance. This is also not a criterion of truth, but a criterion for indisputability. Controversial opinions are usually not called "scientifically accepted" or "scientific", but are often called "unscientific" by opponents. This usually means: "not accepted by the majority of those working in a field".

If something is generally scientifically accepted, i.e. if it remains without any significant and above all socially high-ranking contradiction, it is usually adopted as "scientific information" in textbooks and in public opinion. Then minority opinions are often excluded and ignored until someone who succeeds in formulating contradictions from a comparatively respected position reopens the debate.

In this sense, the assertion that "measles is caused by the measles virus" is undoubtedly a scientifically accepted opinion, which also implies that a measles virus exists and has been proven to be the causative agent. Therefore, Dr. Lanka's view that this "scientific fact" is the result of an error and poor methodology is a minority opinion that would be considered "unscientific" by the majority of scientists. This argumentation is implicitly followed by the expert opinion formulated by Prof. Podbielski, who was appointed in the preliminary proceedings.

Now majority opinion, straight in the science, is not a sufficiently good councellor, even if it is closer to us humans as social beings, and also scientists are social beings, than individually isolated analysis. Historical examples could be given enough to show that and how majority opinions are wrong. Here are some examples.

As early as 2004, Dean pointed out that monocausal thinking is actually obsolete in medicine, especially in infectiology, because the vast majority of infections only develop as an interaction between pathogen and host [2]. However, because the focus on the pathogen is easier, the complexity is overlooked and monocausality continues to be raised to the scientific standard in an abstraction for which there is no responsibility.

For a long time, the doctrine that there are no planets outside our solar system was considered a scientific doctrine in astronomy. Quite a few astronomers had bad chances for advancement if they did not adhere to this dogma. Today several hundred other planets are known.

A more exact analysis of the nourishing debate, particularly in the USA, shows: the danger of saturated fatty acids and superiority of unsaturated fatty acids for disease prevention and preservation of the standard weight, which was majority opinion and a component of official position papers, maintained for decades, collapses at present under the load of contrary data, which were for a long time admits however ignored. The social exclusion mechanisms of the scientific community had led to minority opinions, however well-founded they may be, not being heard [3].

Conversely, it is also known that economic interests often make use of cleverly positioned outsider opinions in order to sow doubt and stop changes that are actually sufficiently well documented scientifically. [4]

The same principle is of course also applied in the other direction: if, as in the health sector, economic interests are very strong, very obvious facts are often overlooked because all those involved react by refusing to perceive them. Because a different view of things, could disturb crucial loyalties and interests [5].

In this respect, in all debates on "scientificity", including this one, one must not forget to look at the social, economic and historical context of the very concept of science that is being used and the values associated with it.

The dependence of methodology on social acceptance and historical circumstances and the need for revision

What is also often overlooked is the following connection: there is no scientific method that would be established once and for all. New methods allow new insights, render old insights obsolete or make them more precise. It is true that the experimental method, which is the main focus here, is a powerful method that has been practiced for a long time. But it is also being refined more and more. For example, in the past a simple comparison was sufficient for a scientifically acceptable publication. This applies to the first three of the works in question here. In the meantime it is standard that comparisons are generated by chance and in many subjects blindness is necessary. As Sheldrake found out in a survey, blinding is not common in basic biological, medical or physical research [6].

While in parapsychology, for example, 85% of all experiments were blind, in basic medical research this was only 6%. This shows that methodological stringency often depends on the awareness of the researchers involved that there is a danger in their field of work that the opinion and attitude of the experimenter may influence the results. Rosenthal has clearly demonstrated this in his experiments for psychology, and by analogy for medicine [7].

Therefore, blindness is common in clinical medical and psychological experiments, but hardly ever in basic research. "Why should it be?" thinks the researcher involved, "we measure objective facts". But even such measurements and perceptions can be due to a wish, as Fleck was able to show with the example of the serological Aquarius reaction [8].

In between, new standards are proposed, but they are only accepted in sub-domains because they are complex and costly. This applies, for example, to systematic, negative controls. A systematic, negative control is when an experimental procedure is repeated in all details without carrying the supposedly causal agent. If, as we will see in this example, the experiment involves a certain form of cell preparation and cultivation, into which nutrient solution is then introduced and finally the presumed causal agent, then a systematic negative control would consist of forming a separate group for each individual step. This is the only way to see whether only the causal agent and not possibly artifacts are really responsible for the results obtained.

To my knowledge, this form of control was introduced by Jan Walleczek and his group [9]. However, it has not spread very much because it is expensive. Interestingly, it is mainly used by researchers working in border areas [10].

The most careful studies from an experimental medical field with systematic negative controls are, to my knowledge, from Garret Yount, [11] Here Johrei healers, a Japanese group, were studied, who allegedly can use "Ki", an immaterial form of energy, to change cancer cells. Because initial pilot experiments were positive, the researchers decided to do careful research. Cancer cell cultures were prepared and treated at a distance by Johrei healers, especially by a master. In systematically negative control experiments, the entire setting was now carried along and built up in the same way. A person was also placed at the same distance and for the same time to record any temperature or electromagnetic effects. The same time and place, the same temperature and humidity were chosen. Systematic negative controls were also performed without a person present, just to record the time factor and variability of the system. Through all these controls the initially positive findings were documented as not stable enough and the "healing effect" was exposed as an artifact.

This example shows that theoretical models that are less accepted by the community usually have to endure much stronger controls in experimental investigations. The strength of the control usually depends on the degree of a priori certainty derived from theoretical model assumptions and unsystematic experience that a given situation is likely to occur. To this extent, this is always also historically conditioned and predetermined by the currently prevailing mainstream. If the general attitude is open-minded and positive, less strong data are sufficient to convince the majority of researchers. In this case, important controls are often omitted.

What is "scientifically proven" is thus not only dictated by the method, but also by the interaction of a currently valid model with methodological considerations and with a priori considerations on the probability of an assumption based on other findings, on prevailing views and on a background theory.

From what has been said, it follows that an experiment or a publication can never provide complete certainty and certainly cannot establish any scientific fact. Rather, this happens in a complex exchange process in which important publications become the source of discourse: they are replicated, they are criticized, they are commented on. And at the end of a complex social negotiation process among experts - much of which does not take place in writing, but in discussions - there is then a "scientific fact".

Therefore, the call for proposals can only be seen as a provocation that calls on the scientific community to reflect. It is interesting to see how a respondent from the mainstream reacts to this provocation by Dr. Lanka. Let's take a closer look at the studies.

The Papers

Study No. 1

Enders, J.F. & Peebles, T.C. (1954) Propagation in tissue cultures of cytopathogenic agents from patients with measles. Proceedings of the Society for Experimental Biology and Medicine, 86(2): 277-286

This study reports on an experimental investigation. Throat swabs, blood samples and stool samples were taken from 7 children who were clinically ill with measles, and biologically processed. These were then treated by suitable procedures in such a way that it could be assumed that bacteria, for example, could no longer be active. The substances were centrifuged and treated with penicillin and streptomycin. In addition, 2 ml sterile, non-fat milk was added. The solution thus obtained was then introduced into various cell cultures and the changes were observed microscopically and compared with untreated cell cultures. The authors found pathological changes manifesting themselves as cell enlargements, suggesting an "immigration" of foreign substances into the cell nucleus, so that the chromatin, i.e. the chromosomes and the supporting molecules surrounding them, are displaced. In addition, inhibitory effects are shown when the infectious isolate has been heated, introduced into other cells and then added to infected cells. Cooling, on the other hand, does not change the infectivity. This indirectly suggests that the foreign substance must be protein.

The authors evaluate their findings as preliminary: "It is our purpose to describe here these observations in a preliminary manner. Additional evidence ... will be sought in future investigations. (p. 278) At the end of their essay they call the data "indirect evidence" (p. 286). This indirect evidence must be supplemented by two more experiments: the direct production of measles in apes and in humans with the material from the tissue cultures.

Methodological remarks and commentary:

The study was conducted on material from 7 children, all of whom had clinical measles. Infectious material could be isolated from 5 children. The material from one child did not cause the pathological changes observed in the material from the other 4 children. Therefore, a 100% infectivity is not given. The authors have certainly tried to avoid mistakes within the framework of the then valid knowledge. Thus, they tried to treat their solutions by adding antibiotics in such a way that bacterial cause of pathological changes could be excluded if possible. However, according to current knowledge, the possibility still remains that resistant strands survived and multiplied during the relatively long incubation period (14-21 days, p. 281). However, the inoculum was filtered through microfilters, which can retain Serratia marcescens, a bacterium, and the inoculum, the authors say, was free of bacteria, which they were able to show by negative growth experiments. It is therefore plausible to assume that no bacteria, at least none known at the time, is responsible for the infectious changes.

However, as the authors themselves state, it could be that other infectious agents in the monkey tissue are responsible, because only monkey tissue has been shown in this and other experiments to be consistently suitable for passing on infectious agents: "only those in which monkeys were employed as the experimental animal have been consistently confirmed by other workers. Great caution should therefore be exercised in the interpretation of any new claims that the virus has been propagated in other hosts or systems. (S. 285)

The authors therefore urge caution, and rightly so. Whether the shortcomings that the authors themselves notice were remedied by themselves or by others in later studies is not the subject of this consideration. Apparently the observations were confirmed by other authors, as reported in Study 2.

It should also be noted that although the experimental solution was treated with various substances - sterilized milk, antibiotics, trypsin, etc. - a control solution containing the same substances without the swabs or sera from blood or stool was not introduced. In this sense the comparisons, although very convincing, are not really equivalent. No systematic negative control was included. Although it is fair to say that this strict control has only become common practice in recent decades - in this respect, the authors worked cleanly according to the standards of the time, otherwise the work would not have been published in a scientific journal - this study cannot be a clear proof that only the swab or sera can be considered for the changes that were observed. At best, it is only suitable as a piece of the mosaic in a larger picture.

It is important to note that the authors still use the term "virus" in this text in the old Latin sense as "infectious agent" or "poison". For this reason, they usually speak of "infectious agent" or "etiologic agent".

In summary, the study proves that cell-changing processes can be generated in cell cultures with material from swabs and blood from children clinically ill with measles. But firstly, this does not happen with all materials. On the other hand, at 2 to 3 weeks, it takes relatively long. Furthermore, the experimental design cannot ensure that only an infectious agent from the sick children's material is really responsible for the changes and not characteristics inherent in the monkey cells under investigation and brought to light by the treatment. Finally, from today's point of view it cannot be excluded that resistant micro-bacteria have led to the observed changes. The term "virus" is used here in a figurative sense. The study cannot therefore provide proof of the existence of a measles virus, but can at best provide an argumentative building block in a necessarily more complex argumentation.

Study No. 2

Bech, V. & von Magnus, P. (1958) Studies on measles virus in monkey kidney tissue cultures. Acta Pathologica Microbiologica Scandinavica 42(1):75-85.

This study essentially replicates the findings of Enders & Peebles (1954) and reports on two further replications that have taken place in the meantime. It is significant for the purposes here that the methodology was essentially repeated. The difference is that the culture media and the suspension media in which the specimens obtained from swabs and blood were stored and grown are different. Again, penicillin and streptomycin were used as antibacterial agents. Isolation of the infectious agent, which is almost throughout this publication reifyingly referred to as "virus", was done by swabs taken from the throat or by gargling with nutrient solution or from blood. The following observations are important for further considerations at this point:

• 13 patients were examined, 5 of them showed positive reactions ("virus recovered"), the other 8 did not.
• Only in one of 11 patients a cultivation from blood could be detected.
• The correlation claimed by the authors of easier detectability at early stages of collection cannot be maintained: 3 of the 5 detected agents are infections that occurred 24 or 18 hours ago, in 2 persons the time is shorter. This is contrasted by negative findings in the 2 other patients where the withdrawal time was less than 24 hours after the start of infection.
• The cytophatological changes that are reported apparently also occur in non-infected monkey kidney tissue and can therefore hardly be described as pathognomonic, which was also described by the other authors: "cytopathic changes similar to those caused by measles virus may be observed also in uninoculated cultures of monkey kidney tissue (Fig. 4-5). These changes are probably caused by virus-like agents, so called 'foamy agents', which seem to be frequently present in kidney cells from apparently healthy monkeys" (p. 80).

Especially the latter observation seems to me to be remarkable, as it points to the unspecificity of exactly those pathological changes that served as the starting point for the optical evidence of an infection in the first publication by Enders & Peebles.

As evidence for the correctness of the thesis that it is a "virus", it is stated that a "complement fixation test" was positive. This was performed on a total of 4 patients. Under the plausible assumption that the patient numbers reported in Table 2 refer to the patients originally reported in Table 1, two of the 4 patients would therefore be among those 4 patients where no virus could originally be isolated, one patient was successful and the fourth patient is new. It remains unclear in how many patients this fixation test was performed with negative results or why not all of them were tested.

Enders & Peebles had warned that only an experimental causation of the disease by isolate in monkeys or humans could prove the causation. Therefore, an infection experiment was performed on two rhesus monkeys bred in the laboratory. One of the two monkeys showed subclinical symptoms. In both cases, a corresponding antibody titer was determined.

Methodological remarks and commentary:

The study suffers in principle from the same weaknesses as the original study by Enders & Peebles:

• It is possible that the changes were caused by resistant strains of bacteria not covered by the antibiotics.
• It is possible that any substances in the solution media are responsible for the changes.
• It is possible that an interaction between the solution medium and the monkey cell leads to the observed change.
• The rate of 5 patients out of 13 is below 50% and thus far from Koch's postulate of 100% infectious causality [12].
• The transmission of the disease to the monkey organism was successful in one of 2 cases. An antibody titre was found in both; a previous infection with measles was excluded. However, on the background of the statement that a "foamy agent" in the kidney cells of the monkeys could just as well be responsible for the change, this statement loses its power of persuasion, since it cannot be excluded that the same "foamy agent" that is naturally present in monkeys could have led to the antibody reaction that was determined.

Linguistically it can be stated that in the course of one year and three publications lying and quoted in between, the opinion that the infectious agent is a "virus" is obviously taken for granted, because practically only the "virus" is still being talked about. This is an interesting example of how reality is created by concepts instead of reality becoming concept-forming.

In summary, this study cannot prove that "the" measles virus exists. What the study shows is that there is an infectious agent that can be detected in less than 50% of cases, but which could just as well have been present in the cells. It could also, overlooked by the authors, have originated somewhere in the breeding media or in the interaction. This could only have been excluded by systematic negative controls, which were not common at that time.

Study No. 3

Nakai, M. & Imagawa, D.T. (1969) Electron microscopy of measles virus replication. Journal of Virology, 3(2): 187-197.

This study provides an electron microscopic description of the infectious agent in question, here already referred to as "measles virus". It describes in the entrance earlier work that would have described orders of magnitude of 100-150 nm or 120-250 nm. Here the different stages of replication of the virus are described. For this purpose the so-called "Edmonston strain" of the virus "propagated in HeLa cells [13]" is used. The literature cited refers to the original work by Enders & Peebles (1954), Study 1 above. The extraction of the virus is not described; the publication allows two interpretations here: 1) The original isolates from Enders & Peebles, which were introduced into cell cultures by them at the time, were also used here. 2) The methods described by Enders & Peebles for obtaining infectious material were also used here. It is difficult to say which of the two interpretations applies. These were introduced into new HeLa cells, mixed with different reagents, further cultivated and purified by four ascending centrifugation steps, obviously with the idea that in the end the lightest particle, the virus, would remain in the filtrate and thus be available for inspection through the microscope. Different, differently shaped structures were found ("the virions are pleomorphic", p. 189), which showed very different sizes from 180 to 600 nm.

The treatment of the controls is not mentioned. The publication only says: "Control preparations of uninoculated HeLa cells were examined in a similar manner" (p. 188). This can be interpreted as meaning that the uninoculated HeLa cells were also subjected to a similar, stepwise centrifugation and were also examined microscopically. This can also be interpreted as meaning that the control cells were provided with the same reagents in the sense of a systematic negative control. However, since this is not mentioned further, and since it can be assumed that it would have been mentioned, since it would have been a costly production step, it cannot be assumed that such systematic negative controls have been generated. Nothing is reported about the findings in control cells. The illustrations show only experimental cells, no controls for comparison.

The authors write that the cytoplasmic inclusion bodies observed by them, i.e. inclusions in the cytoplasm of infected cells, could be related to the formation of new virus particles, but call this speculation, which would have to be confirmed by similar investigations with clear immunological labelling. The same applies to inclusion bodies in the cell nucleus. It is unclear how these are related to a possible virus replication: "The relationship between the nuclear inclusion body and the replication of measles virus is not clear. (S. 196)

Methodological remarks and commentary:

The validity of the study is based on three conditions that are not clear in the context of the publication:

• The study assumes that the Enders & Peebles method is suitable for isolating an infectious agent; in any case, this study is given as a reference for the isolate. Further details on the collection were not given. This may be because the method of collection was generally accepted at the time or simply used here. It remains unclear whether the agent has been newly obtained or has been cultivated in cell lines since Enders & Peebles, i.e. for 15 years.
• The study assumes that only the infectious agent is isolated by the new cultivation of the infectious agent and filtration or centrifugation.
• The study assumes that the reagents that have been added to the HeLa cells to prepare the samples are irrelevant.

Above all, it remains unclear how the putative virus was cultured and propagated in the cells. The authors' choice of words ("The Edmonston [14] strain of measles virus [6 - this refers to Enders & Peebles 1954; publication 1 above], propagated in HeLa cells, was used in this study. p. 187) does not contribute to clarification. This is the only information on how the infectious agent was obtained.

A systematic negative control, i.e. a control condition that was treated in the same way as the experimental cells, including staining, incubation etc., does not seem to have taken place. Instead, apparently untreated cells were simply inspected. What exactly happened to the control cells is not reported. Whether or not structures of a similar kind were found in the control cells is not reported in the publication.

By the way, the size variance of the structures found seems remarkable: previous studies report a size of 100-150 nm, or 120-250 nm. Here, particles of the order of 180-600 nm were found.

In summary, despite the suggestive indications and images, these studies do not provide evidence in the strict sense. Therefore, a systematic negative control should have been performed and it should have been clearly reported that no evidence of similar particles was found in these controls. Now of course a proponent can say that this was self-evident and therefore not worth mentioning. Although such an argumentation is understandable, in the strict sense at least one sentence to this statement would have been necessary here. These facts have one thing in common: namely that it is unclear where the infectious agent came from or how exactly the controls were treated and that it is unclear whether anything was visible in the controls and, if so, what, they make this study useless as an aid to argumentation.

Publication No. 4

Lund, G.A., Tyrrell, D.L.J., Bradley, R.D. & Scraba, D.G. (1984) The molecular length of measles virus RNA and the structural organization of measles nucleocapsids. Journal of General Virology, 65: 1535-1542.

In this study, the structure of the RNA of the measles virus was to be examined by electron microscopy. For this purpose, a virus strain was cultivated and introduced into cells. These were then incubated for 72 hours and after 90-95% of the cells had shown clearly visible cytopathological effects, a purification method was applied. From this, the suspected virus isolate was obtained, which was then further examined. For this purpose, the excess liquid was treated and centrifuged several times, so that ideally the virus would remain. The result was examined by electron microscopy to determine the structure, size and shape of the viral RNA.

Part of the examination is an electron microscopic image of a representative virus (Figure 3a). The authors note that the variety of shape and size ("pleomorphic" p. 1537) already reported by Nakai & Imagawa (1969) was also found here. If Nakai & Imagawa (1969) reported 180-600 nm, particles between 300 and 1000 nm were found here, i.e. about 1.5 times larger than in Nakai & Imagawa. The shown virion has a size of 500nm and is therefore about in the middle of the scattering width.

In addition, structures were visually examined, length measurements were made and the fine structure of the nucleocapsids, i.e. the protein structures containing the viral RNA, was recorded. Calculations on their shape, length and amount within a virion are made, which are not relevant for the present research question.

Methodological remarks and comments:

Control experiments are not reported in this publication. At first glance, this does not seem necessary either, but it also reveals the potential weakness of the entire chain of argumentation. This publication is based on the assumption that by infection and cultivation a virus can indeed be isolated, which can then be characterized and further investigated. If this assumption is correct, then the shape, size and diversity of the measles virus reported here is indeed proven. If it is wrong, the properties reported here belong to a different particle.

This shows that the publication, as is common practice in science, is based on the cumulative truth in literature, i.e. on previous experiments and works. This is time-saving and in a certain way useful. But it also obviously increases the error dependence. If, purely hypothetically, cell components had been transported from cells by the reported procedure, then all analyses would refer to such components, which would then be (mis)interpreted as virus particles. Such an oversight could only be ruled out if a single, unambiguous, systematically negative control, i.e. a control procedure in which all steps (enrichment, incubation, staining, addition of reagents and nutrient solution) were performed without the original inoculation with presumably infectious material. However, at least in the literature available here, this has not been done.

Therefore, it could be purely theoretical that what is visible here is not a virus from the measles isolate, but e.g. one that is contained in the cell lines and has been further cultivated, or a mixture of these. Since the observed particles are "pleiomorphic", i.e. they can have many different shapes and sizes, the question of whether a particle can be assigned to a specific virus population is probably not so easy to answer.

The discussion is reminiscent of that reported by Ludwik Fleck, who first had the syphilis spirochetes generated as a fact by means of the Aquarius reaction and various staining techniques [15]. Fleck came to the conclusion that a scientific fact is an agreement. Similarly, it can be assumed that it is an agreement to call the particles found a measles virus. An "objective", methodologically independent fact can hardly be justified by this. For this would require that an important requirement in this publication - or in previous publications on which this publication is based - had been fulfilled, which cannot be detected in the texts presented here:

Systematic negative controls must have been carried out, which could have ruled out that the propagated, cultured and multiplied components actually came from the virus isolate and not from the cell cultures themselves. After all, there is the theoretical possibility, which has been repeatedly advocated by a minority [16], that cancer cells themselves contain infectious agents, such as bacteria or viruses. If this were the case, they would be further cultivated and isolated by the cultivation and enrichment methods used here, just like the inoculum introduced.

It seems obvious to me that the picture shown in Figure 3 of this publication shows a particle containing RNA that has been measured, characterized and described in detail. However, it is not clear whether this particle originates from the measles inoculum or from the cells themselves. The fact that this is not discussed as a problem can mean two things:

1. There is one publication in which this has been done and to which all other publications refer. The ones discussed above are certainly not among them, and no proof of this alleged possibility is evident in any text so far.
2. It has not yet been recognized as a methodological problem.

It seems to me that 2) is the most probable variant: if there were methodological awareness of the problem, then every author who publishes on this topic would feel compelled to cite the corresponding reference or would refer to it with a sentence in the methods or discussion section. Since this does not happen, the problem was most likely either not recognized or, if recognized, not found relevant.

In summary, this study does present a clear picture that can be addressed as a virus particle. However, both the diversity and size variance of the image, together with the lack of systematic negative control in all studies, raise doubts that the image offered is indeed a picture of a measles virus. Only a morphological analysis of the many forms and a clear characterization, e.g. based on immunological methods, and above all a robust proof, that these cannot be cultivations from cell cultures, would dispel any doubt.

Publication No. 5

Horikami, S.M. & Moyer, S.A. (1995) Structure, transcription, and replication of mesles virus. In: V. ter Meulen & M.A. Billeter (Eds) Measles Virus. Current Topics in Microbiology and Immunology 191 (pp. 35-50). Springer: New York, Heidelberg.

This work brings together almost 120 other papers in one overview and deals exclusively with the structure of viral RNA, gene coding and related studies. Thus, it presupposes that the question of interest here has been answered and is in itself not relevant to the question of interest here. It shows, however, that a very rich research network has been established by researchers who all work under the consensus that the viruses isolated here are indeed derived from measles. The correctness of this assumption is neither discussed nor problematized, but is obviously assumed. Thus the factuality is substantiated. Whether or not the details of the explanations for specialists contain indications that gene sequences or the behaviour of RNA are typical for certain viruses is beyond my competence. However, it is clear: nothing is said in this review about the method of isolating the virus itself and the methodological validity of this very first step. Rather, this is assumed to be a methodical matter of course. Whether or not this is the case cannot be determined on the basis of these and the previously discussed publications. Formally, it should perhaps be considered: even if Springer is a very good publisher, such edited works are more likely to be subject to a gentle review.

Publication No. 6.

Daikoku, E., Morita, C., Kohno, T. & Sano, K. (2007) Analysis of morphology and infectivity of measles virus particles. Bulletin of the Osaka Medical College, 53(2): 107-114.

This study analyzed morphology and infectivity of measles virus particles. At the outset, the authors note that several other studies have concluded, including those discussed above, that the infectious agent is polymorphic and has been observed in various sizes between 180 and 600 nm, and 300 and 1000 nm, respectively. Furthermore, the separability into three fractions was reported. This will be continued here. The Edmonston strain is also used, without any further information about the extraction. Various cells, including those of monkeys, but also human cell lines are infected with it. These are incubated and cultivated for 7 days before infected cells are obtained by centrifugation and microfiltration. They are subjected to electron microscopy, both conventional and with immunological labelling.

As in the other studies, polymorphic particles were found to be measles viruses. They have sizes from 50 nm to 950 nm. All particles in any size formation are infectious. Most of the particles have a size of 300 to 500 nm and are thus in the range of the size range observed by others. Particles can be labeled with different immunological methods and thus show different fine structures.

Methodical remarks and comment:

Formally, it should be noted that the "Bulletin of the Osaka Medical College" is a rather peripheral journal, which at the moment cannot even come up with an impact factor. Even some journals that publish largely in German such as "Der Schmerz", "Der Psychotherapeut" or "Forschende Komplementärmedizin" have impact factors, which shows that their work is cited by other authors. The self-description of the journal on its website suggests that there is no peer review, only an internal examination. The journal is mainly used by members of the Osaka Medical College to communicate their findings. It is therefore not a "high-level" publication, and one might have expected that a groundbreaking finding such as the clear electron microscopic description would be published in a more widely distributed journal.

The study, like all others, rests on the acceptance and validity of the extraction method. Therefore, we have the same problem as with all other studies: the extraction of the isolate follows the known scheme. Here it is presented even more briefly: "MeV, the Edmonston strain, was inoculated....". (p. 108). With "MeV" short for "measles virus" and "the Edmonston strain", the tradition of research in this field is served.

We saw in publication No. 3 that the same wording was used and a reference to the original study by Enders & Peebles (1954) was used, which is omitted here. So we can assume that again either the same method as Enders & Peebles was used for virus cultivation or, more likely, that the infected cell line from that time was used to obtain the isolate. This means, however, that everything that has happened and has not happened since then is happening or has not happened at all. This may involve the introduction and further cultivation of another agent, or the further propagation of substances or agents in the cell cultures. Since no systematic negative control has been made, this cannot be decided here either. As convincing as the images and analyses are, and as suggestive as the research tradition is: it cannot be ruled out that an infectious agent of another nature or cell-own components from the measles culture were isolated and depicted here. The short statement "MeV, the Edmonston strain..." does not allow a decision to be made. Control experiments are not mentioned.

Therefore, this study is ultimately not suitable for answering the present question.

Discussion and consequences

What do we learn from this situation? To summarize: none of the studies performs a really solid negative control, which ensures that the potentially infectious agent is not already present in the starting material, the monkey kidney cells or the HeLa cells. Both the introduced agents themselves, or these in interaction with the cell material, or this alone, or all together with the isolate from the diseased tissue could be responsible for the observed changes.

In this sense, the challenger, Dr. Lanka, seems to me to be right: a single study will not prove the existence of the measles virus, and certainly not one of the studies presented here.

But why then the consensus in science, which obviously feels disturbed in its business by such a troublemaker as Lanka? This can be seen from the expert opinion of Prof. Podbielski, who points out that the picture is only possible if all findings are considered together, including the studies not discussed in this process.

Science is always a cumulative social process. In the course of the entire infectiological theory-building process, the consensus emerged that measles must be an infectious process. Somehow everyone expected that it would be possible to isolate something like a virus. So the a priori expectation was high that a study would have to have such a result at some point. And thus the entirety of the researchers looks to some extent benevolently over the methodological weaknesses of the first studies away, even if their authors admonish for caution. By the citation tradition suddenly facticity is produced, which also - if they would be present - later negative studies cannot revise so simply any longer.

This was recently demonstrated very impressively by an example where a wrong theory was supported for years, even though there were sufficient negative findings, simply because the most powerful authors supported the wrong theory and systematically suppressed negative findings. It was the theory that a certain form of myositis was caused by amyloid deposits. Only many publications later and after a great deal of effort did it become clear, on the one hand, that the theory was wrong and, on the other hand, that this wrong opinion was due to the fact that facts had been created by citation networks [17].

This factuality becomes the more difficult to doubt the longer it is handed down and the longer it is accepted by everyone. Yes, but: "there are all these genetic studies, all these electron microscopic studies," the proponent will say. Correct. The question that Lanka has raised, and which seems quite justified, is: were the very first data, to which all later studies refer, really collected in such a way that they undoubtedly isolated only the suspected causal agent? As we have seen, this is not the case. In the first studies - and none of the other studies presented eliminated the shortcoming - no negative controls were included. Therefore, agents already present in the monkey cells, the famous "foamy agent", agents created by interaction, agents introduced by the additives or agents created by interaction with the HeLa cells or a mixture of these could be responsible for the observed subsequent changes. Since all later methods and studies seem to be based on these first studies, the argument does not seem to be invalidated.

It could be eliminated by presenting a study that eliminates the problem. Either there is no such study, or the plaintiff did not find it and did not submit it.

This is an interesting situation. I am curious how the court will decide. Actually, from my point of view the following should happen now:

A really good laboratory would have to carry out the isolation of the suspected measles virus from scratch and, with the help of systematic negative controls, carry out a culture that shows that the accompanying procedures - nutrient solution, cell insertion, transfer to a cell strain - do not lead to infectivity and the observed changes, and then subsequently characterize the virus electron microscopically and biochemically. This study would have to be registered beforehand and a high-ranking journal would have to arrange for its publication regardless of the result.

Or else, a knowledgeable researcher should pull the publication from the files in which this happened. The submitted publications do not accomplish this task. It is more likely that everyone will go back to business as usual, because questioning a consensus that has lasted almost half a century is quite costly.

The measles virus process can perhaps give us a little food for thought. The discourse will only be properly initiated when a really well-off virologist accepts this challenge. Perhaps Mr. Lanka should take his money and audition in a really good laboratory and arrange such a study there? Maybe that would help. But here too I am skeptical. Because: science is socially conditioned and is subject to the same weaknesses as all other social interactions. And here too, with enough chutzpah and persistence, the majority opinion can be challenged if one is prepared to take the beating that is initially to be expected. Whether a change will occur afterwards depends on two factors:

• whether one is actually right and it turns out that the majority has been wrong so far, and
• whether it is possible to get a spokesman to speak this truth who finds enough ears.

We can be curious. We are currently witnessing a historical process in which truth is being negotiated. With his challenge Lanka has pointed out that consensual truth is less certain than it seems. With his response, Bardens has tried to meet the challenge. The studies presented, as the analyses above show, are less strong than one might think. The fact that this does not call into question the fact that measles can be dangerous, that vaccinations may help, etc., is not addressed at all. What is under discussion is the majority consensus that what has happened in science so far is sufficient to prove the factuality of the measles virus. After all I have seen so far, this seems doubtful to me. In view of the great replication problem in medicine [18] and the resulting doubt in society, it would probably be wise if a few competent researchers were to set out to dispel these doubts by careful replications. Once and for all. Or to reopen the books. At the moment, both seems possible to me, but nothing has yet been definitively proven.

Translated & reblogged Version - Original here

Telegraph main page with overview of all articles: Link

Visit our Telegram Channel for additional news & information: Link

Chat with like-minded in our Telegram Chat Group: Link

Please support to keep this blog alive: paypal

Sources and references

[1] Announcement of the Klein-Klein-Verlag from 24.11.2011

[2] Dean, K. (2004). The role of methods in maintaining orthodox beliefs in health research. Social Science and Medicine, 58, 675-685.

[3] The debate has been competently presented by a science journalist. Even if not everything is accurately represented, the historical debate is of great importance: Teicholz, N. (2014) The Big Fat Surprise. Why Butter, Meat and Cheese Belong in a Healthy Diet. New York: Simon and Schuster. For example, the largest randomized low-fat diet study ever conducted, involving nearly 50,000 women over 7 years of age, shows that these long standard diets and scientifically proven nutritional advice are useless for both weight loss and the prevention of heart attacks: Beresford, S. A., Johnson, K. C., Ritenbaugh, C., Lasser, N. L., Snetselaar, L. G., Black, H. R., et al. (2006). Low-fat dietary pattern and risk of colorectal cancer: The women`s health initiative randomized controlled dietary modification trial. Journal of the American Medical Association, 295(6), 643-654. Howard, B. V., Manson, J. E., Stefanick, M. L., Beresford, S. A., Frank, G. R., Jones, B., et al. (2006). Low fat dietary pattern and weight change over 7 years: The Women’s Health Initiative dietary modification trial. Journal of the American Medical Association, 295(1), 39-49. Howard, B. V., van Horn, L., Hsia, J., Manson, J. E., Stefanick, M. L., Wassertheil-Smoller, S., et al. (2006). Low fat dietary pattern and risk of cardiovascular disease: The Women’s Health Initiative randomized controlled dietary modification trial. Journal of the American Medical Association, 295, 655-666.

[4] Hudson, L., & Jacot, B. (1986). The outsider in science: a selective review of evidence, with special reference to the Nobel prize. In C. Bagley & G. K. Verma (Eds.), Pesonality, Cognition, and Values (pp. 3-23). London: Macmillan.

[5] Gøtzsche has worked this out for the pharmaceutical industry: Gøtzsche, P. C. (2013). Deadly Medicines and Organised Crime: How Big Pharma Has Corrupted Health Care. London: Radcliff.

[6] Sheldrake, R. (1998). Experimenter effects in scientific research: How widely are they neglected? Journal of Scientific Exploration, 12, 73-78.

[7] Rosenthal, R. (1976). Experimenter Effects in Behavioral Research (enlarged edition). New York: Irvington.

[8] Fleck, L. (1980). Origin and development of a scientific fact. Introduction to the teaching of thinking style and thinking collective. With an introduction edited by L. Schäfer and T. Schnelle. Frankfurt: Suhrkamp. (Original published 1935).

[9] Walleczek, J., Shiu, E. C., & Hahn, G. M. (1999). Increase in raditiation-induced HPRT gene mutation frequency after nonthermal exposure to nonionizing 60Hz electromagnetic fields. Radiation Research, 151, 489-497.

[10] Stefan Baumgartner, for example, who does research with potentiated, serial ultra-high diluted substances on plants, has basically carried out all his experiments with systematic negative controls and most researchers in this field have done the same for him. Cf. approximately Scherr, C., Simon, M., Spranger, J., & Baumgartner, S. (2009). Effects of potentised substances on growth rate of the water plant Lemna gibba L. Complementary Therapies in Medicine, 17, 63-70, oder Witt, C. M., Bluth, M., Albrecht, H., Weisshuhn, T. E. R., Baumgartner, S., & Willich, S. N. (2007). The in vitro evidence for an effect of high homeopathic potencies – A systematic review of the literature. Complementary Therapies in Medicine, 15, 128-138, die einen Überblick geben.

[11] Radin, D., Taft, R., & Yount, G. (2004). Effects of healing intention on cultured cells and truly random events. Journal of Alternative and Complementary Medicine, 10, 103-112. Taft, R., Moore, D., & Yount, G. (2005). Time-lapse analysis of potential cellular responsiveness to Johrei, a Japanese healing technique. BMC Complementary and Alternative Medicine, 5(1), 2. Yount, G., Smith, S., Avanozian, V., West, J., Moore, D., & Freinkel, A. (2004). Biofield perception: A series of pilot studies with cultured human cells. Journal of Alternative and Complementary Medicine, 10, 463-467.

[12] However, Koch's postulates are no longer upheld, because it has been seen that they are far too mechanistic. This change in the historical context alone is highly interesting, since it shows that we have implicitly moved away from the monocausal scheme, which, however, we try to maintain in the general perception by speaking of "pathogens", "causative agents", etc.

[13] HeLa cells are cell cultures from the carcinoma from which Henrietta Lacks died in 1951 and which have been cultivated and commercially available since then.

[14] This is obviously the name of the boy from whom this first infectious substance was obtained.

[15] Fleck, L. (1980). Origin and development of a scientific fact. Introduction to the teaching of thinking style and thinking collective. With an introduction edited by L. Schäfer and T. Schnelle. Frankfurt: Suhrkamp. (Original published 1935).

[16] Lynes, B. (2011, orig. 1987). The Cancer Cure That Worked! Fifty Years of Suppression. Lake Tahoe: Biomed Publishing.

Kevles, D. J. (1997). Pursuing the unpopular: A history of courge, viruses, and cancer. In R. B. Silver (Ed.), Hidden Histories of Science (pp. 69-112). London: Granta Books. Vor allem der letztere Text zeigt: jede spätere Mainstream-Theorie der Krebsforschung wurde zunächst als Aussenseitertheorie heftigst bekämpft, bevor sie akzeptiert wurde.

[17] Greenberg, S. A. (2009). How citation distortions create unfounded authority: analysis of a citation network. British Medical Journal, 339, b2680

[18] Horton, R. (2015). Offline: What is medicine’s 5 sigma? Lancet, 385, 1380